Ljubica Matic

Ljubica Matic

Senior Forskare | Docent

Molekylärbiolog med fokus på att utveckla nya läkemedel och biomarkörer för kärlsjukdomar

E-postadress: ljubica.matic@ki.se
Telefon: +46852482726
Besöksadress: Karolinska Institutet, BioClinicum J8:20, Visionsgatan 4, 17164 Solna
Postadress: K1 Molekylär medicin och kirurgi, K1 MMK Kärlkirurgi Translationell vaskulär medicin, 171 77 Stockholm
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Om mig

  • Ljubica Matic är Docent i molekylär medicin och huvudforskare vid avdelningen för Kärlkirurgi vid Karolinska Institutet. Hon tog sin magisterexamen i molekylärbiologi från Belgrads universitet, Serbien, och en doktorsexamen i medicinsk biokemi från Karolinska Institutet år 2012. Sedan 2019 är hon gruppledare för Translationell Kärlmedicin vid Centrum för molekylär medicin, KI, med fokus på translationell forskning om nya terapeutiska och diagnostiska mål för behandling av hjärt-kärlsjukdomar, särskilt ateroskleros och restenoskomplikationer.


    Hennes arbete har under åren uppmärksammats med bidrag och utmärkelser från Vetenskapsrådet, Hjärt-Lungfonden, Svenska Sällskapet för Medicinsk Forskning, KI Faculty Consolidator-bidrag, American Heart Association (Daniel Steinberg Early Career Investigator-priset 2023) och Kungliga Vetenskapsakademien (Sven och Ebba Hagberg-priset 2019). Hon är KI:s huvudforskare för flera pågående EU Horizon-projekt, samt Leducq-nätverket ATHENA och La Caixa-projektet AtheroPTM. Ljubica Matic arbetar som expertgranskare för Vetenskapsrådet, Hjärt-Lungfonden, European Research Council, British och Dutch Heart Foundations, Danska kardiovaskulära akademin, etc. Hon är vald till ledamot i European Society of Cardiology (FESC), styrelseledamot för KI Research Incubator (KIRI), medlem i Women’s Leadership Committee i International Society of Applied Cardiovascular Biomedicine och medlem i ledningskommittén för EU:s COST-actions AtheroNET och CardioPharmaGENET.

    Hennes redaktionella arbete inkluderar positioner som redaktionsledamot för tidskriften Vascular Pharmacology och associerad redaktör för tidskriften Atheroclerosis. Hon har >110 publikationer med över 5500 citeringar och h-index 46.

Forskningsbeskrivning

  • Matic-gruppen (https://linktr.ee/ljubicamatic) använder innovativa, integrerade in silico-pipelines för utforskning av Biobank of Karolinska Endarterectomy (BiKE, est. 2002), Biobank of Karolinska lower extremity Peripheral Arterial Disease (BiKPAD, est. 2025) och Biobank of Karolinska Smooth Muscle Cells (BiKSMC, est. 2024), för att identifiera mål relaterade till glatta muskelceller som har ett direkt orsakssamband med mänsklig kärlsjukdom. Målupptäckt via AI/ML-styrda multimodala dataintegrationer följs av fenotypning, utmaning och proof-of-concept interventionsstudier i murina kärlskador och sjukdomsmodeller, samt in vitro-undersökningar med primära mänskliga glatta muskelceller.


    Med denna tvärvetenskapliga metod är hennes uppdrag att skapa en kraftfull plattform för extrapolering av grundläggande forskningsresultat till de olika områdena av klinisk hjärt-kärlsjukdom. För detta ändamål samarbetar hon med Big Pharma och är meduppfinnare av totalt 21 patent, vilket accelererar utvecklingen från målupptäckt till patientbehandlingar.

Undervisning

  • Sedan 2004 har Ljubica Matic kontinuerligt ägnat 20 % av sin tid åt pedagogiskt arbete som föreläsare, handledare och kursledare för doktorander inom hjärt-kärlprogrammet och studenter på grundnivå inom medicin- och biomedicinprogrammen vid KI. Sedan 2013 har hon varit kursansvarig för doktorandkursen i Kärlcellbiologi, Hjärt-kärlprogrammet, KI. Sedan 2021 är hon biträdande kursansvarig för KI:s masterprogram i Global Biomedicin, valbart spår i Cirkulation, metabolism och endokrinologi.

    Under åren har hon även organiserat fristående internationella doktorandkurser i hjärt-kärlsjukdomar inom ramen för EU:s Horizon Marie Sklodowska-Curie ITN-projekt, EU:s ERASMUS-program, samt kurser i guldstandard för biobankspraxis för EU:s Widera-program.

Artiklar

Alla övriga publikationer

Forskningsbidrag

  • Swedish Heart-Lung Foundation
    1 januari 2026 - 31 december 2027
    Background: Smooth muscle cells (SMCs) are the main structural vessel component. In cardiovascular diseases (CVD) underlined by atherosclerosis, the balance of excessive vs insufficient SMC activation, along with their plasticity, determines the vessel healing response. SMCs functionally trans-differentiate elicited by pathological stimuli into multiple subphenotypes, which critically affects atherosclerotic plaque vulnerability. Yet, there are currently no CVD therapies specifically targeting SMCs. Hypothesis and aims: Our rationale is that a deep exploration of the pathways controlling SMC subphenotypes in plaques can lead to novel strategies to support their healing capacity. We seek to 1) discover druggable targets that regulate SMC plasticity and 2) evaluate the implementation of SMC therapies, beyond the current best available treatments. Workplan: We will develop novel integrative pipelines for in silico exploration of a large atherosclerosis biobank to identify SMC targets by: a) multi-omics data integration, b) deconvolved by single-cell RNA signatures of SMC subphenotypes, c) stratified by clinical parameters and d) enriched with genetic CVD association data. SMC targets will be investigated mechanistically in vitro and their druggability evaluated via proof-of-concept in vivo models in mice. Significance: With this translational approach, the project is poised to push the basic knowledge frontier about SMC subphenotypes in human lesions and pave the way for a paradigm shift in clinical treatment of complex CVDs.
  • Swedish Heart-Lung Foundation
    1 januari 2025 - 31 december 2027
    Background: Smooth muscle cells (SMCs) are the main structural vessel component. In cardiovascular diseases (CVD) underlined by atherosclerosis, the balance of excessive vs insufficient SMC activation, along with their plasticity, determines the vessel healing response. SMCs functionally trans-differentiate elicited by pathological stimuli into multiple subphenotypes, which critically affects atherosclerotic plaque vulnerability. Yet, there are currently no CVD therapies specifically targeting SMCs. Hypothesis and aims: Our rationale is that a deep exploration of the pathways controlling SMC subphenotypes in plaques can lead to novel strategies to support their healing capacity. We seek to 1) discover druggable targets that regulate SMC plasticity and 2) evaluate the implementation of SMC therapies, beyond the current best available treatments. Workplan: We will develop novel integrative pipelines for in silico exploration of a large atherosclerosis biobank to identify SMC targets by: a) multi-omics data integration, b) deconvolved by single-cell RNA signatures of SMC subphenotypes, c) stratified by clinical parameters and d) enriched with genetic CVD association data. SMC targets will be investigated mechanistically in vitro and druggability evaluated via proof-of-concept in vivo models. Finally, we will test complementation of current therapies with SMC-targeted plaque stabilisation in small and large animal models, to alleviate total disease burden. Significance: With this translational approach, the project will push the basic knowledge frontier about SMC subphenotypes in human lesions and pave the way for a paradigm shift in clinical treatment of complex CVDs.
  • European Commission
    1 oktober 2024 - 30 september 2027
    There are over 330 million people living on the planet affected by one of over 6,000 identified genetic rare diseases (RD). They urgently need timely diagnosis and development of specific treatments. Although Europe leads the way in RD research, there is a clear gap in research and innovation (R&I) between countries. To bridge this gap, networking and knowledge sharing between IMGGE (Institute of Molecular Genetics and Genetic Engineering, Serbia) and 3 world-class counterparts at EU level - KI (Karolinska Institute, Sweden), CNAG (National Center for Genomic Analysis, Spain) and UAM (Autonomous University of Madrid, Spain) is envisioned. BRIDGING-RD’s objectives are: (1) upgrade the IMGGE RD Biobank to reach full interoperability of genetic and phenotypic data in order to increase participation in transnational research and innovation projects related to human health
    (2) upgrade bioinformatics pipelines specific to RD to increase the rate of solved RD cases in IMGGE’s RD Biobank
    (3) upgrade capacity for modelling of metabolic diseases as well as capacity to test small molecule drugs, in order to increase the number of translational studies
    (4) upgrade research support offices in order to increase success in obtaining funds from research and/or innovation agencies, industry, foundations etc. Objectives will be achieved through staff exchanges, expert visits, trainings or workshops, conference attendance, joint summer schools and dissemination/outreach activities. Crucially, an exploratory R&I project, engaging all partners will focus on identifying an innovative drug, pharmacochaperone, for a selected metabolic RD. BRIDGING-RD will have impact by significantly improving the scientific excellence and innovation capacity of IMGGE, raising its research reputation and research management skills. It will also impact networking and mobility of qualified scientists in the RD field, thus boosting creativity and ultimately enhancing economic growth at the European level.
  • Swedish Heart-Lung Foundation
    1 januari 2024 - 31 december 2025
  • Swedish Heart-Lung Foundation
    1 januari 2024 - 31 december 2026
    Background: Smooth muscle cells (SMCs) are the main structural vessel component. In cardiovascular diseases (CVD) underlined by atherosclerosis, the balance of excessive vs insufficient SMC activation, along with their plasticity, determines the vessel healing response. SMCs functionally trans-differentiate elicited by pathological stimuli into multiple subphenotypes, which critically affects atherosclerotic plaque vulnerability. Yet, there are currently no CVD therapies specifically targeting SMCs. Hypothesis and aims: Our rationale is that a deep exploration of the pathways controlling SMC subphenotypes in plaques can lead to novel strategies to support their healing capacity. We seek to 1) discover druggable targets that regulate SMC plasticity and 2) evaluate the implementation of SMC therapies, beyond the current best available treatments. Workplan: We will develop novel integrative pipelines for in silico exploration of a large atherosclerosis biobank to identify SMC targets by: a) multi-omics data integration, b) deconvolved by single-cell RNA signatures of SMC subphenotypes, c) stratified by clinical parameters and d) enriched with genetic CVD association data. SMC targets will be investigated mechanistically in vitro and druggability evaluated via proof-of-concept in vivo models. Finally, we will test complementation of current therapies with SMC-targeted plaque stabilisation in small and large animal models, to alleviate total disease burden. Significance: With this translational approach, the project will push the basic knowledge frontier about SMC subphenotypes in human lesions and pave the way for a paradigm shift in clinical treatment of complex CVDs.
  • Swedish Research Council
    1 januari 2024 - 31 december 2026
    Smooth muscle cells (SMCs) are the main structural vessel component. In cardiovascular diseases (CVD) underlined by atherosclerosis, the balance of excessive vs insufficient SMC activation, along with their plasticity, determines the vessel healing response. SMCs functionally trans-differentiate elicited by pathological stimuli into multiple subphenotypes, which critically affects plaque vulnerability. Yet, there are currently no CVD therapies specifically targeting SMCs. Our hypothesis is that exploration of pathways controlling SMC subphenotypes can lead to novel strategies to support their healing capacity. We seek to 1) discover druggable targets that regulate SMC plasticity and 2) evaluate the implementation of SMC therapies, beyond the best available treatments. We will develop in silico exploration of a large atherosclerosis biobank to identify SMC targets by: a) multi-omics data integration, b) deconvolved by single-cell RNA signatures of SMC subphenotypes, c) stratified by clinical parameters and d) enriched with genetic CVD association data. SMC targets will be investigated mechanistically in vitro and druggability evaluated via proof-of-concept in vivo models. We will test complementation of current therapies with SMC-targeted plaque stabilisation, to alleviate total disease burden.With this translational approach, the project will push the knowledge frontier about SMC subphenotypes in human lesions and pave the way for a paradigm shift in treatment of complex CVD.
  • European Commission
    1 januari 2024 - 31 december 2027
    Healthcare is the fasted growing EU27 expenditure. Personalised medicine, comprising tailored approaches for prevention, diagnosis, monitoring and treatment is essential to reduce the burden of disease and improve the quality of life. Integration of multiple data types (multimodal data) into artificial intelligence models is required for the development of accurate and personalised interventions. This is particularly true for the inclusion of genomic data, which is information-rich and individual-specific, and more routinely available as the cost of sequencing continues to fall. Multimodal data integration is complex due to privacy & governance requirements, the presence of multiple standards, distinct data formats, and underlying data complexity and volume. NextGen tools will remove barriers in data integration several cardiovascular use cases. NextGen deliverables will include tooling for multimodal data integration and research portability, extension of secure federated analytics to genomic computation, more effective federated learning over distributed infrastructures, more effective and accessible tools for genomic data analysis
    improved clinical efficiency of variant prioritisation
    scalable genomic data curation
    and improved data discoverability and data management. A comprehensive gap analysis of the existing landscape, factoring ongoing initiatives will ensure NextGen deliverables are forward-looking and complementary. NextGen embedded governance framework and robust regulatory processes will ensure secure multi-jurisdictional multiomic multimodal data access aligned with initiatives including “1+ Million Genomes” and the European Health Data Space. Several real-world pilots will demonstrate the effectiveness of NextGen tools and will be integrated in the NextGen Pathfinder network of five collaborating clinical sites as a self-contained data ecosystem and comprehensive proof of concept.
  • Swedish Heart-Lung Foundation
    1 januari 2022 - 31 december 2024
  • Swedish Research Council
    1 januari 2022 - 31 december 2025
  • Swedish Heart-Lung Foundation
    1 januari 2021 - 31 december 2023
  • Swedish Heart-Lung Foundation
    1 januari 2021 - 31 december 2021
  • Swedish Heart-Lung Foundation
    1 januari 2021 - 31 december 2023
  • Swedish Heart-Lung Foundation
    1 januari 2021 - 31 december 2021
  • Swedish Research Council
    1 januari 2020 - 31 december 2023
  • Swedish Heart-Lung Foundation
    1 januari 2019 - 31 december 2020
  • Swedish Heart-Lung Foundation
    1 januari 2019 - 31 december 2020
  • Swedish Heart-Lung Foundation
    1 januari 2018 - 31 december 2020
  • Swedish Research Council
    1 januari 2018 - 31 december 2021

Anställningar

  • Senior Forskare, Molekylär medicin och kirurgi, Karolinska Institutet, 2022-
  • Graduate researcher, Institute for Molecular Genetics and Genetic Engineering, 2002-2003

Examina och utbildning

  • Docent, Molekylär medicin, Karolinska Institutet, 2021
  • Medicine Doktorsexamen, Institutionen för medicinsk biokemi och biofysik, Karolinska Institutet, 2012

Nyheter från KI

Kalenderhändelser från KI