Eckardt Treuter
Professor
E-mail: eckardt.treuter@ki.se
Visiting address: Blickagången 16, 14152 Flemingsberg
Postal address: H7 Medicin, Huddinge, H7 GUT Treuter, 171 77 Stockholm
About me
- Eckardt Treuter has been leading a research team as a professor at the Karolinska Institutet since 2007. He has more than three decades research experience in the regulation of gene expression, epigenomics, nuclear receptor signalling, metabolic and inflammatory disease pathways. He has completed his PhD at the Martin Luther University Halle-Wittenberg in Germany with a dissertation about stress-regulated transcription factors. He did his postdoc at the Karolinska Institutet where he identified nuclear receptor-associated proteins using unbiased screenings. Since then the study of these proteins, many of which are now known as fundamental transcriptional coregulators, has remained his key interest.
Research
- Epigenetic control of metabolism and inflammation by transcriptional coregulators
Our research aims at better understanding how the epigenome controls metabolic and inflammatory pathways in the context of obesity, type 2 diabetes, fatty liver disease and atherosclerosis. Epigenetic alterations that trigger changes in epigenome activity and gene expression are fundamental reprogramming events that contribute to the development of these diseases. However, the underlying regulatory mechanisms, the critical components, and the causal relationship of these associations are currently poorly defined. With an emphasis on so-called coregulators we address these issues utilizing a multidisciplinary approach, including molecular biology, biochemistry, genomics and epigenomics approaches, genetically modified cell, tissue and mouse models, and collaborations with clinicians to study human material. We also develop proof-of-concept models for the therapeutic targeting of epigenome components, such as chromatin-modifying complexes and enhancers.
Transcription factors (>1600) and associated coregulators (>300) play central roles in linking epigenome alterations to transcriptional reprogramming, as they shape the chromatin/enhancer landscape (i.e. the epigenome) and determine signal responses. Although these processes are well studied for many transcription factors and coactivators, our understanding of the precise roles of corepressors is currently lacking behind. It is further poorly understood whether and how the dysregulation of specific coregulators contributes to, or potentially even causes, disease.
Our search for candidates that might be particularly relevant for metabolic and inflammatory disease pathways revealed a potential key role of a fundamental corepressor complex, consisting of the core subunits histone deacetylase HDAC3, G-protein pathway suppressor 2 (GPS2), and the related corepressors NCOR and SMRT. Although these subunits were originally identified as nuclear receptor-associated proteins, we know today that the complex controls many other transcription factors and multiple cellular pathways. Our studies have demonstrated the involvement of the complex in the regulation of cholesterol metabolism and transport, in anti-inflammatory crosstalk mechanisms, in adipose tissue inflammation and hypertrophy, and in hepatic fatty acid oxidation and lipogenesis. Intriguingly, alterations of GPS2 expression in adipocytes and macrophages associate with systemic inflammation and diabetic risk in obese humans, suggesting the identified pathways to be conserved and clinically relevant. Thus, our current hypothesis is that inappropriate complex function, in part due to altered expression and modification of the core subunit GPS2, triggers epigenetic reprogramming and thereby alters the susceptibility to metabolic-inflammatory signals that contribute to disease.
We now attempt to evaluate the hypothesis using a variety of genetically modified disease models, and in response to different dietary and pharmacological interventions. For example, we have begun to investigate the role of corepressor-mediated epigenome alterations in monocytes/macrophages in linking type 2 diabetes to the progression of atherosclerosis. In another project, we would like to understand how post-translational modifications of individual subunits modulate epigenomic and transcriptional activities of the corepressor complex (and postulated sub-complexes), and how these modifications change in response to different signals and during the development of type 2 diabetes, atherosclerosis and fatty liver disease.
Besides a better understanding of coregulator-mediated epigenome alterations during the development of metabolic-inflammatory diseases, we also expect novel insights into epigenetic memory and crosstalk mechanisms between metabolic ‘master’ cell types such as macrophages, adipocytes and hepatocytes. These insights may help to develop novel epigenome-based strategies for the prevention and treatment of metabolic-inflammatory diseases.
Articles
- Article: CELL METABOLISM. 2025;37(2):460-476.e8Lin K; Wei L; Wang R; Li L; Song S; Wang F; He M; Pu W; Wang J; Wazir J; Cao W; Yang X; Treuter E; Fan R; Wang Y; Huang Z; Wang H
- Article: ADVANCED SCIENCE. 2024;11(20):2307201de la Rosa JV; Tabraue C; Huang Z; Orizaola MC; Martin-Rodriguez P; Steffensen KR; Zapata JM; Bosca L; Tontonoz P; Alemany S; Treuter E; Castrillo A
- Article: SCIENCE ADVANCES. 2024;10(1):eadi2689Ludzki AC; Hansen M; Zareifi D; Jalkanen J; Huang Z; Omar-Hmeadi M; Renzi G; Klingelhuber F; Boland S; Ambaw YA; Wang N; Damdimopoulos A; Liu J; Jernberg T; Petrus P; Arner P; Krahmer N; Fan R; Treuter E; Gao H; Ryden M; Mejhert N
- Article: JOURNAL OF CLINICAL INVESTIGATION. 2023;133(20):e169671Wang T; Dong Y; Huang Z; Zhang G; Zhao Y; Yao H; Hu J; Tueksammel E; Cai H; Liang N; Xu X; Yang X; Schmidt S; Qiao X; Schlisio S; Stromblad S; Qian H; Jiang C; Treuter E; Bergo MO
- Journal article: NATURE. 2023;619(7968):E24Paredes A; Justo-Mendez R; Jimenez-Blasco D; Nunez V; Calero I; Villalba-Orero M; Alegre-Marti A; Fischer T; Gradillas A; Sant'Anna VAR; Were F; Huang Z; Hernansanz-Agustin P; Contreras C; Martinez F; Camafeita E; Vazquez J; Ruiz-Cabello J; Area-Gomez E; Sanchez-Cabo F; Treuter E; Bolanos JP; Estebanez-Perpina E; Ruperez FJ; Barbas C; Enriquez JA; Ricote M
- Article: NATURE. 2023;618(7964):365-373Paredes A; Justo-Mendez R; Jimenez-Blasco D; Nunez V; Calero I; Villalba-Orero M; Alegre-Marti A; Fischer T; Gradillas A; Sant'Anna VAR; Were F; Huang Z; Hernansanz-Agustin P; Contreras C; Martinez F; Camafeita E; Vazquez J; Ruiz-Cabello J; Area-Gomez E; Sanchez-Cabo F; Treuter E; Bolanos JP; Estebanez-Perpina E; Ruperez FJ; Barbas C; Enriquez JA; Ricote M
- Article: NUCLEIC ACIDS RESEARCH. 2023;51(3):1067-1086Huang Z; Efthymiadou A; Liang N; Fan R; Treuter E
- Article: STAR PROTOCOLS. 2022;3(2):101338Huang Z; Wang C; Treuter E; Fan R
- Article: ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY. 2022;42(5):659-676Rykaczewska U; Zhao Q; Saliba-Gustafsson P; Lengquist M; Kronqvist M; Bergman O; Huang Z; Lund K; Waden K; Pons Vila Z; Caidahl K; Skogsberg J; Vukojevic V; Lindeman JHN; Roy J; Hansson GK; Treuter E; Leeper NJ; Eriksson P; Ehrenborg E; Razuvaev A; Hedin U; Matic L
- Article: MOLECULAR CELL. 2021;81(5):953-968.e9Huang Z; Liang N; Goni S; Damdimopoulos A; Wang C; Ballaire R; Jager J; Niskanen H; Han H; Jakobsson T; Bracken AP; Aouadi M; Venteclef N; Kaikkonen MU; Fan R; Treuter E
- Article: MOLECULAR METABOLISM. 2020;42:101066Barilla S; Liang N; Mileti E; Ballaire R; Lhomme M; Ponnaiah M; Lemoine S; Soprani A; Gautier J-F; Amri E-Z; Le Goff W; Venteclef N; Treuter E
- Article: CELL REPORTS. 2020;32(11):108141Drareni K; Ballaire R; Alzaid F; Goncalves A; Chollet C; Barilla S; Nguewa J-L; Dias K; Lemoine S; Riveline J-P; Roussel R; Dalmas E; Velho G; Treuter E; Gautier J-F; Venteclef N
- Article: NATURE COMMUNICATIONS. 2019;10(1):1684Liang N; Damdimopoulos A; Goni S; Huang Z; Vedin L-L; Jakobsson T; Giudici M; Ahmed O; Pedrelli M; Barilla S; Alzaid F; Mendoza A; Schroder T; Kuiper R; Parini P; Hollenberg A; Lefebvre P; Francque S; Van Gaal L; Staels B; Venteclef N; Treuter E; Fan R
- Article: FASEB JOURNAL. 2019;33(2):1631-1643Huang Z; Liang N; Damdimopoulos A; Fan R; Treuter E
- Article: CELL REPORTS. 2019;26(4):984-995.e6Becares N; Gage MC; Voisin M; Shrestha E; Martin-Gutierrez L; Liang N; Louie R; Pourcet B; Pello OM; Luong TV; Goni S; Pichardo-Almarza C; Roberg-Larsen H; Diaz-Zuccarini V; Steffensen KR; O'Brien A; Garabedian MJ; Rombouts K; Treuter E; Pineda-Torra I
- Journal article: ONCOGENE. 2019;38(2):299-300Zhu J; Zhao C; Kharman-Biz A; Zhuang T; Jonsson P; Liang N; Williams C; Lin C-Y; Qiao Y; Zendehdel K; Stromblad S; Treuter E; Dahlman-Wright K
- Article: METHODS IN MOLECULAR BIOLOGY. 2019;1951:167-178Liang N; Fan R; Goñi S; Treuter E
- Article: CELL REPORTS. 2018;24(11):2957-2971.e6Drareni K; Ballaire R; Barilla S; Mathew MJ; Toubal A; Fan R; Liang N; Chollet C; Huang Z; Kondili M; Foufelle F; Soprani A; Roussel R; Gautier J-F; Alzaid F; Treuter E; Venteclef N
- Journal article: DIABETES & METABOLISM. 2017;43(2):a34Drareni K; Toubal A; Al azaid F; Ballaire R; Barilla S; Foufelle F; Treuter E; Venteclef N
- Article: NATURE MEDICINE. 2016;22(7):780-791Fan R; Toubal A; Goni S; Drareni K; Huang Z; Alzaid F; Ballaire R; Ancel P; Liang N; Damdimopoulos A; Hainault I; Soprani A; Aron-Wisnewsky J; Foufelle F; Lawrence T; Gautier J-F; Venteclef N; Treuter E
- Article: MUCOSAL IMMUNOLOGY. 2014;7(6):1416-1428Jakobsson T; Vedin L-L; Hassan T; Venteclef N; Greco D; D'Amato M; Treuter E; Gustafsson J-A; Steffensen KR
- Article: ONCOGENE. 2014;33(34):4340-4351Zhu J; Zhao C; Kharman-Biz A; Zhuang T; Jonsson P; Liang N; Williams C; Lin C-Y; Qiao Y; Zendehdel K; Stroemblad S; Treuter E; Dahlman-Wright K
- Journal article: DIABETES & METABOLISM. 2013;39:a101Venteclef N; Clément K; Treuter E; Toubal A
- Article: JOURNAL OF CLINICAL INVESTIGATION. 2013;123(1):362-379Toubal A; Clement K; Fan R; Ancel P; Pelloux V; Rouault C; Veyrie N; Hartemann A; Treuter E; Venteclef N
- Article: PLOS ONE. 2012;7(3):e32080Ehrlund A; Jonsson P; Vedin L-L; Williams C; Gustafsson J-A; Treuter E
- Article: BMC GENOMICS. 2012;13:50Genome-wide landscape of liver X receptor chromatin binding and gene regulation in human macrophagesPehkonen P; Welter-Stahl L; Diwo J; Ryynanen J; Wienecke-Baldacchino A; Heikkinen S; Treuter E; Steffensen KR; Carlberg C
- Journal article: ENDOCRINOLOGY. 2011;152(7):2542-2545Damdimopoulou P; Treuter E
- Journal article: CELL RESEARCH. 2011;21(5):711-714Treuter E
- Article: GENES & DEVELOPMENT. 2010;24(4):381-395Venteclef N; Jakobsson T; Ehrlund A; Damdimopoulos A; Mikkonen L; Ellis E; Nilsson L-M; Parini P; Janne OA; Gustafsson J-A; Steffensen KR; Treuter E
- Article: HUMAN MOLECULAR GENETICS. 2009;18(15):2802-2812Massinen S; Tammimies K; Tapia-Paez I; Matsson H; Hokkanen M-E; Soderberg O; Landegren U; Castren E; Gustafsson J-A; Treuter E; Kere J
- Article: MOLECULAR CELL. 2009;34(4):510-518Jakobsson T; Venteclef N; Toresson G; Damdimopoulos AE; Ehrlund A; Lou X; Sanyal S; Steffensen KR; Gustafsson J-A; Treuter E
- Article: MOLECULAR AND CELLULAR BIOLOGY. 2009;29(8):2230-2242Ehrlund A; Anthonisen EH; Gustafsson N; Venteclef N; Remen KR; Damdimopoulos AE; Galeeva A; Pelto-Huikko M; Lalli E; Steffensen KR; Gustafsson J-A; Treuter E
- Article: BIOCHEMISTRY. 2008;47(18):5205-5215Burendahl S; Treuter E; Nilsson L
- Article: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA. 2007;104(40):15665-15670Sanyal S; Bavner A; Haroniti A; Nilsson L-M; Lundasen T; Rehnmark S; Witt MR; Einarsson C; Talianidis I; Gustafsson J-A; Treuter E
- Article: BIOCHEMICAL JOURNAL. 2007;406(2):343-353Matthews J; Wihlen B; Heldring N; MacPherson L; Helguero L; Treuter E; Haldosen L-A; Gustafsson J-A
- Article: NEUROSCIENCE. 2007;146(2):604-616Galeeva A; Treuter E; Tomarev S; Pelto-Huikko M
- Article: JOURNAL OF BIOLOGICAL CHEMISTRY. 2007;282(14):10449-10455Heldring N; Pawson T; McDonnell D; Treuter E; Gustafsson J-A; Pike ACW
- Article: MOLECULAR AND CELLULAR BIOLOGY. 2007;27(4):1407-1424Fang S; Miao J; Xiang L; Ponugoti B; Treuter E; Kemper JK
- Journal article: MOLECULAR CELL. 2007;25(2):178-180Treuter E; Gustafsson J-A
- Article: JOURNAL OF MEDICINAL CHEMISTRY. 2006;49(25):7357-7365Roelens F; Heldring N; Dhooge W; Bengtsson M; Comhaire F; Gustafsson J-A; Treuter E; De Keukeleire D
- Article: NUCLEIC ACIDS RESEARCH. 2005;33(11):3561-3569Båvner A; Matthews J; Sanyal S; Gustafsson JA; Treuter E
- Article: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA. 2005;102(10):3593-3598Kong EH; Heldring N; Gustafsson J; Treuter E; Hubbard RE; Pike ACW
- Article: JOURNAL OF BIOLOGICAL CHEMISTRY. 2004;279(37):38721-38729Damdimopoulos AE; Miranda-Vizuete A; Treuter E; Gustafsson J; Spyrou G
- Article: PLANT CELL. 2004;16(6):1521-1535Bharti K; von Koskull-Döring P; Bharti S; Kumar P; Tintschl-Körbitzer A; Treuter E; Nover L
- Article: EMBO REPORTS. 2004;5(6):613-619Steffensen KR; Holter E; Båvner A; Nilsson M; Pelto-Huikko M; Tomarev S; Treuter E
- Article: MOLECULAR AND CELLULAR BIOLOGY. 2004;24(8):3445-3459Heldring N; Nilsson M; Buehrer B; Treuter E; Gustafsson J
- Article: MOLECULAR ENDOCRINOLOGY. 2004;18(2):312-325Sanyal S; Matthews J; Bouton D; Kim HJ; Choi HS; Treuter E; Gustafsson J
- Article: BIOLOGY OF REPRODUCTION. 2003;69(2):508-517Liu DL; Liu WZ; Li QL; Wang HM; Qian D; Treuter E; Zhu C
- Article: MOLECULAR AND CELLULAR BIOLOGY. 2003;23(12):4187-4198Tazawa H; Osman W; Shoji Y; Treuter E; Gustafsson J; Zilliacus J
- Article: MOLECULAR AND CELLULAR BIOLOGY. 2003;23(4):1260-1268Antonson P; Schuster GU; Wang L; Rozell B; Holter E; Flodby P; Treuter E; Holmgren L; Gustafsson J
- Article: JOURNAL OF BIOLOGICAL CHEMISTRY. 2002;277(51):49761-49766Borgius LJ; Steffensen KR; Gustafsson J; Treuter E
- Article: MOLECULAR ENDOCRINOLOGY. 2002;16(9):2065-2076Brendel C; Schoonjans K; Botrugno OA; Treuter E; Auwerx J
- Article: EUROPEAN JOURNAL OF NEUROSCIENCE. 2002;16(4):671-683Galeeva A; Treuter E; Tuohimaa P; Pelto-Huikko M
- Article: JOURNAL OF BIOLOGICAL CHEMISTRY. 2002;277(24):21862-21868Wärnmark A; Treuter E; Gustafsson J; Hubbard RE; Brzozowski AM; Pike ACW
- Article: EMBO REPORTS. 2002;3(5):478-484Båvner A; Johansson L; Toresson G; Gustafsson J; Treuter E
- Article: MOLECULAR ENDOCRINOLOGY. 2002;16(3):515-528Holter E; Kotaja N; Mäkela S; Strauss L; Kietz S; Jänne OA; Gustafsson J; Palvimo JJ; Treuter E
- Article: JOURNAL OF BIOLOGICAL CHEMISTRY. 2001;276(26):23397-23404Differential recruitment of the mammalian mediator subunit TRAP220 by estrogen receptors ERα and ERβWärnmark A; Almlöf T; Leers J; Gustafsson J; Treuter E
- Article: MOLECULAR ENDOCRINOLOGY. 2001;15(4):501-511Zilliacus J; Holter E; Wakui H; Tazawa H; Treuter E; Gustafsson J
- Article: JOURNAL OF BIOLOGICAL CHEMISTRY. 2000;275(51):39855-39859Zhang H; Thomsen JS; Johansson L; Gustafsson J; Treuter E
- Article: JOURNAL OF BIOLOGICAL CHEMISTRY. 2000;275(8):5308-5317Caira F; Antonson P; Pelto-Huikko M; Treuter E; Gustafsson J
- Article: PLANT CELL. 2000;12(2):265-278Döring P; Treuter E; Kistner C; Lyck R; Chen A; Nover L
- Article: MOLECULAR AND CELLULAR BIOLOGY. 2000;20(4):1124-1133Johansson L; Båvner A; Thomsen JS; Färnegårdh M; Gustafsson J; Treuter E
- Article: JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY. 1999;71(3-4):93-102Windahl SH; Treuter E; Ford J; Zilliacus J; Gustafsson J; McEwan IJ
- Article: MOLECULAR ENDOCRINOLOGY. 1999;13(7):1105-1118Wiebel FF; Steffensen KR; Treuter E; Feltkamp D; Gustafsson J
- Article: JOURNAL OF BIOLOGICAL CHEMISTRY. 1999;274(25):18121-18127Subramaniam N; Treuter E; Okret S
- Article: JOURNAL OF BIOLOGICAL CHEMISTRY. 1999;274(10):6667-6677Treuter E; Johansson L; Thomsen JS; Wärnmark A; Leers J; Pelto-Huikko M; Sjöberg M; Wright APH; Spyrou G; Gustafsson JA
- Article: JOURNAL OF BIOLOGICAL CHEMISTRY. 1999;274(1):345-353Johansson L; Thomsen JS; Damdimopoulos AE; Spyrou G; Gustafsson J; Treuter E
- Article: MOLECULAR AND CELLULAR BIOLOGY. 1998;18(10):6001-6013Leers J; Treuter E; Gustafsson J
- Article: MOLECULAR ENDOCRINOLOGY. 1998;12(6):864-881Treuter E; Albrektsen T; Johansson L; Leers J; Gustafsson J
- Article: MOLECULAR GENETICS AND GENOMICS. 1997;255(3):322-331Boscheinen O; Lyck R; Queitsch C; Treuter E; Zimarino V; Scharf KD
- Article: PLANTA. 1997;202(1):117-125Lyck R; Harmening U; Hohfeld I; Treuter E; Scharf KD; Nover L
- Show more
All other publications
- Preprint: BIORXIV. 2025Efthymiadou A; Gu C; Wang C; Wang H; Li Z; Garcia-Irigoyen O; Fan R; Treuter E; Huang Z
- Review: OBESITY. 2021;29(12):2013-2025Barilla S; Treuter E; Venteclef N
- Review: FRONTIERS IN ENDOCRINOLOGY. 2019;10:411Liang N; Jakobsson T; Fan R; Treuter E
- Book chapter: HANDBOOK OF NUTRITION, DIET, AND EPIGENETICS. 2019;p. 233-263Alzaïd F; Jakobsson T; Treuter E; Venteclef N
- Book chapter: HANDBOOK OF NUTRITION, DIET, AND EPIGENETICS. 2018;p. 1-31Alzaïd F; Jakobsson T; Treuter E; Venteclef N
- Review: FEBS LETTERS. 2017;591(19):2959-2977Treuter E; Fan R; Huang Z; Jakobsson T; Venteclef N
- Conference publication: DIABETOLOGIA. 2017;60:S261Drareni K; Barilla S; Alzaid F; Ballaire R; Treuter E; Venteclef N
- Preprint: BIORXIV. 2017Becares N; Gage MC; Martin-Gutierrez L; Shrestha E; Louie R; Pourcet B; Pello OM; Luong TV; Goñi S; Liang N; Pichardo C; Røberg-Larsen H; Diaz V; Steffensen KR; Garabedian MJ; Rombouts K; Treuter E; Pineda-Torra I
- Book chapter: COMPENDIUM OF INFLAMMATORY DISEASES. 2016;p. 994-1016Venteclef N; Jakobsson T; Treuter E
- Review: HANDBOOK OF EXPERIMENTAL PHARMACOLOGY. 2016;233:95-135Giudici M; Goni S; Fan R; Treuter E
- Other: M S-MEDECINE SCIENCES. 2014;30(1):15-18Toubal A; Treuter E; Venteclef N
- Review: TRENDS IN ENDOCRINOLOGY AND METABOLISM. 2013;24(12):625-634Toubal A; Treuter E; Clement K; Venteclef N
- Book chapter: ENCYCLOPEDIA OF INFLAMMATORY DISEASES. 2013;p. 1-24Venteclef N; Jakobsson T; Treuter E
- Review: TRENDS IN PHARMACOLOGICAL SCIENCES. 2012;33(7):394-404Jakobsson T; Treuter E; Gustafsson J-A; Steffensen KR
- Review: JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY. 2012;130(3-5):169-179Ehrlund A; Treuter E
- Conference publication: DIABETES & METABOLISM. 2012;38:A30-A31Toubal A; Allili R; Pelloux V; Barsh G; Clement K; Treuter E; Venteclef N
- Review: BIOCHIMICA ET BIOPHYSICA ACTA: INTERNATIONAL JOURNAL OF BIOCHEMISTRY AND BIOPHYSICS. 2011;1812(8):909-918Treuter E; Venteclef N
- Review: TRENDS IN ENDOCRINOLOGY AND METABOLISM. 2011;22(8):333-343Venteclef N; Jakobsson T; Steffensen KR; Treuter E
- Review: PHYSIOLOGICAL REVIEWS. 2007;87(3):905-931Heldring N; Pike A; Andersson S; Matthews J; Cheng G; Hartman J; Tujague M; Stroem A; Treuter E; Warner M; Gustafsson J-A
- Corrigendum: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA. 2006;103(21):8298Kong EH; Heldring N; Gustafsson J; Treuter E; Hubbard RE; Pike ACW
- Review: TRENDS IN ENDOCRINOLOGY AND METABOLISM. 2005;16(10):478-488Båvner A; Sanyal S; Gustafsson J; Treuter E
- Review: MOLECULAR ENDOCRINOLOGY. 2003;17(10):1901-1909Wärnmark A; Treuter E; Wright APH; Gustafsson J
- Review: PHYSIOLOGICAL REVIEWS. 2001;81(4):1535-1565Nilsson S; Mäkelä S; Treuter E; Tujague M; Thomsen J; Andersson G; Enmark E; Pettersson K; Warner M; Gustafsson J
- Review: NOVARTIS FOUNDATION SYMPOSIUM. 2000;230:7-14Treuter E; Warner M; Gustafsson JA
- Review: HORMONES AND AGING. 1998;54:121-166Sorensen HN; Treuter E; Gustafsson JA
- Other: ARCHIVES OF TOXICOLOGY. SUPPLEMENT. ARCHIV F�R TOXIKOLOGIE. SUPPLEMENT. 1998;20:21-28Gustafsson JA; Kuiper G; Enmark E; Treuter E; Rafter J
- Book chapter: RESULTS AND PROBLEMS IN CELL DIFFERENTIATION. 1994;p. 125-162Scharf KD; Materna T; Treuter E; Nover L
- Show more
Grants
- Role of monocyte enhancers and silencers in inflammatory type 2 diabetesNovo Nordisk Foundation1 January 2024 - 31 December 2025Type 2 diabetes (T2D) is a heterogenous disease with chronic inflammation being a feature of recently identified T2D subtypes. Suspected major drivers of these inflammatory subtypes are monocytes. An intriguing hypothesis is that monocytes acquire epigenetic changes (not encoded by the genome DNA) in response to diverse metabolic-inflammatory signals already at early diabetic stages. This establishes a memory that pre-disposes monocytes to further trigger the inflammatory T2D state and its complications including cardiovascular diseases. To shed light on the underlying mechanisms, we will study the role of so-called enhancers and silencers, regulatory elements that control how genes are turned on and off, in monocytes. Our studies may help to overcome a knowledge gap as the monocyte enhancer and silencer landscape and its T2D-associated alterations are currently unknown. Such alterations may become translational important as they may lead to new targets for T2D treatment. _x000D_ _x000D_ _x000D_ _x000D_
- Swedish Research Council1 January 2023 - 31 December 2026The purpose of our research is to contribute to a deeper understanding of closely linked transcriptional and epigenetic mechanisms underlying health and disease. We are particularly interested in the role of coregulators, which via controlling transcription factors and chromatin states are essential components of these mechanisms.With an emphasis on a fundamental corepressor complex implicated in metabolic and inflammatory disease pathways, we recently made the unexpected discovery that corepressors operate at both enhancers and silencers to trigger alternative macrophage gene expression programs.Here we propose research within three aims to address the following key hypotheses emerging from this discovery:Corepressors are essential components of topologically associating domains (TADs) to control chromatin dynamics and transcription, in cooperation with transcription factors and other coregulators.Corepressors mark TAD-intrinsic silencers in different signaling contexts and can be exploited for genome-wide silencer screenings.Corepressor alterations trigger epigenetic remodeling and memory mechanisms that causally link type 2 diabetes to cardiovascular diseases such as atherosclerosis.
- Role of transcriptional corepressors in epigenetic mechanisms underlying atherosclerosis and nonalcoholic fatty liver diseaseNovo Nordisk Foundation1 January 2023 - 31 December 2023
- Swedish Cancer Society1 January 2022Epigenetic changes play a decisive role in the development of cancer and are assumed to be a cause of increased cancer risk in metabolic diseases such as fatty liver and cardiovascular diseases and also in obesity. Epigenetics means on top of genetics and deals with modifications of the genetic material that do not change the DNA sequence in the genome. These modifications determine where and when genes are turned on or off and can be part of an epigenetic memory that affects the cells' function and communication with the environment. It is likely that epigenetic differences are a reason why individual people are at different risk of developing cancer in connection with metabolic diseases. Our project aims to identify epigenetic mechanisms and changes that contribute to liver cancer associated with obesity and non-alcoholic fatty liver disease, which are established risk factors. Our unique approach is to study two key components: regulatory DNA elements that control gene expression, and proteins that bind to these elements and influence the structure and function of the genome. We will apply the latest genome-wide methods to map epigenetic changes in different cell types in the liver (hepatocytes, macrophages), both in mouse models and in human liver cells, in collaboration with clinical researchers. We hope that our research results will contribute to a deeper understanding of the mechanisms that link metabolic diseases and cancer, especially liver cancer, where knowledge of epigenetic causes of disease is currently completely lacking. Although our research is pre-clinical, we will bring new knowledge and methodology that will benefit patients. Our results can, for example, lead to new diagnosis methods by identifying epigenetic biomarkers, and to new forms of therapy by stimulating the development of new drugs that counteract epigenetic changes that cause cancer.
- Role of transcriptional corepressors in epigenetic mechanisms underlying atherosclerosis and non-alcoholic fatty liver diseaseNovo Nordisk Foundation1 January 2022 - 31 December 2022
- Role of transcriptional corepressors in epigenetic mechanisms underlying atherosclerosis and non-alcoholic fatty liver diseaseNovo Nordisk Foundation1 January 2021 - 31 December 2021
- Swedish Research Council1 December 2020 - 31 December 2022
- On the role of non-coding RNAs in the epigenomic regulation of metaflammationNovo Nordisk Foundation1 January 2018 - 31 December 2020
- How changes in the epigenome contribute to metabolic diseases and cancers - from basic mechanisms to therapeutic strategiesSwedish Cancer Society1 January 2018The onset of metabolic diseases such as obesity, diabetes, fatty liver and cardiovascular disease are related to changes in metabolism but also have inflammatory causes. Inflammation is believed to be an important factor linking metabolic diseases and various cancers. Recent years of research suggest that changes within the epigenome, through chromatin modifications linked to gene expression, play a crucial role. Individual differences in the structure and function of the epigenome can be a reason why individual people react differently to similar nutritional and environmental challenges in developing metabolic diseases and cancer. Our studies aim to better understand how changes in the epigenome contribute to an inflammatory disease environment. In addition, we try to develop concept models for future therapeutic treatments by modifying the epigenome's components. To achieve these goals, we focus on two key components: "coregulators" i.e. proteins that affect the structure and function of the epigenome, and ‘enhancers’, i.e. cell type-specific enhancers of gene expression. We will apply modern genomic methods to map the epigenome in various disease processes in mice as well as in human tissues, through collaboration with clinical researchers. We hope that our research results will contribute to a deeper understanding of the intricate relationships between metabolic diseases, inflammation and cancer at the molecular and physiological level. In addition, we hope that our concept models will have therapeutic significance for the development of new drugs that can counteract or correct disease-related epigenomal changes.
- Epigenomic mechanisms underlying metaflammation - towards a better understanding and treating inflammation in the context of obesity and type 2 diabetesNovo Nordisk Foundation1 January 2017 - 1 January 2018
- How obesity and related metabolic diseases can cause cancer:from mouse models to new strategies to prevent and treat cancerSwedish Cancer Society1 January 2017The onset of metabolic diseases such as obesity, diabetes and arteriosclerosis are related to changes in metabolism, but also have inflammatory causes. The disease-related correlation between metabolism and inflammation is referred to as metaflammation and is today a fundamental risk factor for the development of various cancers. Recent years of research suggest that changes within the epigenome, through chromatin modifications linked to gene expression, play a crucial role. Epigenomic differences are thought to be an important reason why individuals react differently to similar nutritional and environmental challenges in developing cancer. Our research aims to better understand how epigenomic processes shape a metaflammatory disease environment, and vice versa, and can lead to cancer. We try to answer these questions by studying co-regulators, proteins that modify chromatin in conjunction with transcription factors, in tissue-specific knockout mouse models and in human tissue. We will apply and develop modern genomic strategies, particularly ChIP sequencing, to map the epigenome in various disease pathways in mice as well as in human tissue and isolated cell types. In addition to basic biomedical research, we plan to expand our clinical collaboration. We hope that our research results will contribute to a deeper understanding of the intricate relationships between metabolism, inflammation and cancer at the molecular and physiological level. In addition, we hope that the project will open up new opportunities to treat and prevent metabolic diseases and cancer. The GPS2 complex is one of the first examples of an anti-inflammatory coregulator that can modify the epigenome and whose expression and function are affected by metabolic diseases. This could lead to therapeutic possibilities to counteract metaplasty by restoring the function of the complex and thereby inhibiting the development of cancer.
- Swedish Research Council1 January 2017 - 31 December 2020
- How obesity and related metabolic diseases can cause cancer:from mouse models to new strategies to prevent and treat cancerSwedish Cancer Society1 January 2016The onset of metabolic diseases such as obesity, diabetes and arteriosclerosis are related to changes in metabolism, but also have inflammatory causes. The disease-related correlation between metabolism and inflammation is referred to as metaflammation and is today a fundamental risk factor for the development of various cancers. Recent years of research suggest that changes within the epigenome, through chromatin modifications linked to gene expression, play a crucial role. Epigenomic differences are thought to be an important reason why individuals react differently to similar nutritional and environmental challenges in developing cancer. Our research aims to better understand how epigenomic processes shape a metaflammatory disease environment, and vice versa, and can lead to cancer. We try to answer these questions by studying co-regulators, proteins that modify chromatin in conjunction with transcription factors, in tissue-specific knockout mouse models and in human tissue. We will apply and develop modern genomic strategies, particularly ChIP sequencing, to map the epigenome in various disease pathways in mice as well as in human tissue and isolated cell types. In addition to basic biomedical research, we plan to expand our clinical collaboration. We hope that our research results will contribute to a deeper understanding of the intricate relationships between metabolism, inflammation and cancer at the molecular and physiological level. In addition, we hope that the project will open up new opportunities to treat and prevent metabolic diseases and cancer. The GPS2 complex is one of the first examples of an anti-inflammatory coregulator that can modify the epigenome and whose expression and function are affected by metabolic diseases. This could lead to therapeutic possibilities to counteract metaplasty by restoring the function of the complex and thereby inhibiting the development of cancer.
- How obesity and related metabolic diseases can cause cancer:from mouse models to new strategies to prevent and treat cancerSwedish Cancer Society1 January 2015The onset of metabolic diseases such as obesity, diabetes and arteriosclerosis are related to changes in metabolism, but also have inflammatory causes. The disease-related correlation between metabolism and inflammation is referred to as metaflammation and is today a fundamental risk factor for the development of various cancers. Recent years of research suggest that changes within the epigenome, through chromatin modifications linked to gene expression, play a crucial role. Epigenomic differences are thought to be an important reason why individuals react differently to similar nutritional and environmental challenges in developing cancer. Our research aims to better understand how epigenomic processes shape a metaflammatory disease environment, and vice versa, and can lead to cancer. We try to answer these questions by studying co-regulators, proteins that modify chromatin in conjunction with transcription factors, in tissue-specific knockout mouse models and in human tissue. We will apply and develop modern genomic strategies, particularly ChIP sequencing, to map the epigenome in various disease pathways in mice as well as in human tissue and isolated cell types. In addition to basic biomedical research, we plan to expand our clinical collaboration. We hope that our research results will contribute to a deeper understanding of the intricate relationships between metabolism, inflammation and cancer at the molecular and physiological level. In addition, we hope that the project will open up new opportunities to treat and prevent metabolic diseases and cancer. The GPS2 complex is one of the first examples of an anti-inflammatory coregulator that can modify the epigenome and whose expression and function are affected by metabolic diseases. This could lead to therapeutic possibilities to counteract metaplasty by restoring the function of the complex and thereby inhibiting the development of cancer.
- Mechanisms of anti-inflammatory nuclear receptor signaling in metabolic diseases and cancerSwedish Cancer Society1 January 2014The onset of metabolic diseases such as obesity, diabetes, arteriosclerosis and various cancers have metabolic and inflammatory (metaplastic) components. Recent years of research indicate that nuclear receptors (proteins that bind metabolites and hormones and regulate gene expression) play a crucial role in metaflammatory signaling pathways and can inhibit inflammatory gene expression. In addition, co-regulators (proteins that modify chromatin) link nuclear receptor signaling to epigenomic mechanisms. Obviously, deeper insights into anti-inflammatory signaling pathways are of utmost importance for therapeutic intervention. Our research focuses on fundamental issues regarding anti-inflammatory nuclear receptor signaling and disease mechanisms. We have recently discovered a protein (GPS2) within the corepressor complex of importance for the link between metabolism and inflammation via nuclear receptors. We now want to move on to show the relevance of "metaflammatory" disease mechanisms. We will use tissue-specific GPS2 knockout mice, experimental disease and cancer models, and genome-wide techniques. We also want to investigate the interaction between the GPS2 network with the estrogen receptor and inflammatory signaling in breast cancer. The proposed research will lead to a better understanding of how changes in nuclear receptor signaling, their anti-inflammatory networks, and their interactions with the epigenome can alter gene expression and thus contribute to the onset of metabolic diseases and cancer. In addition, we hope that the results from the project will have therapeutic significance for the development of new anti-inflammatory drugs. For example, one could imagine that drugs that specifically affect the interaction between core receptors and corepressors will counteract inflammation and thus inhibit the development and progression of cancer.
- Swedish Research Council1 January 2013 - 31 December 2016
- Swedish Research Council1 January 2012 - 31 December 2015
- Epigenomic control of metabolism and inflammation by nuclear receptors and coregulators - link to metaflammatory disease pathwaysNovo Nordisk Foundation26 August 2011
- Swedish Research Council1 January 2009 - 31 December 2011
Employments
- Professor, Department of Medicine, Huddinge, Karolinska Institutet, 2024-
Degrees and Education
- Docent, Karolinska Institutet, 2005