Rongrong Fan

Rongrong Fan

Principal Researcher | Docent
Visiting address: Blickagången 16, 14152 Flemingsberg
Postal address: H7 Medicin, Huddinge, H7 GUT Fan, 171 77 Stockholm
Part of:

About me

  • Lab page:
    https://ki.se/en/bionut/liver-and-monocyte-remodelling-in-non-alcoholic-fatty-liver-disease-and-cardiovascular

    Research grants:

    Swedish research council (Vetenskapsrådet)

    EFSD / Novo Nordisk Future Leaders Award 
    Cancerfonden

    The Rolf Luft Grant for Instrumentation 
    SRP diabetes 
    KI faculty-funded senior researcher 
    CIMED
    NOVO NORDISK Foundation
    KI Doctoral funding
    Åke Wibergs Stiftelse
    Diabetes Wellness Sverige Foundation
    EFSD / Lilly research fellowship
    KI foundation

    Commission of trust:
    Editorial board: Frontiers in Endocrinology 2021-.
    Guest editor: Frontiers in Endocrinology 2020-2021.
    Steering Committee: lipoprotein research networks in KI south campus
    (supported by CIMED).
    Grant evaluation task for: ANR, VR, FWF, KID, etc
    Invited reviewer in: Nat Com, JCI, eLife, JBC, FASEB J, Diabetologia, etc.
    Organizing committee and chairs for domestic and international conferences.

Research

  • My research combines the phenotypic/clinical analysis with multi-OMICs approaches to understand the fundamental question of how over-nutritional
    signals alter chromatin remodelling to promote metabolic disease development. We have so far analyzed different patient samples in the transcriptomic, cistromic and epigenomic levels and identified a group of interesting candidates involved in species-conserved and disease-relevant regulation of glucose and lipid metabolism. Of particular interest is the transcription factor coregulator GPS2, the dysregulation of which is associated with de-repressed inflammation and impaired lipid oxidation pathways, leading to type 2 diabetes and liver disease progression.
    The ongoing research activity involves further investigation of the coregulator-based mechanisms in the genomic and epigenomic level in various
    disease contexts. Understanding such pathways is crucial for better deciphering disease mechanisms which is ultimately required for identifying
    novel targets with diagnostic and intervention potential.

Teaching

  • Main supervisor of 3 ongoing PhD student and 1 postdoc
    Cosupervisor of 1 ongoing PhD student and 2 completed PhD students
    Project supervisor of 5 bachelor students and 2 Master student
    More than 200 teaching hours in Bachelor, Master and PhD courses

    Master level course director
    Professional university pedagogy training (equivalent to more than 5 weeks)

Articles

All other publications

Grants

  • Swedish Cancer Society
    1 January 2024
    Liver cancer is dangerous. It is difficult to treat and is even resistant to the latest immunotherapy. When liver cancer progresses to advanced stages, the patient's 5-year survival rate is very low. It is therefore important to understand why liver cancer is difficult to eliminate and what helps cancer cells escape our immune surveillance. Such knowledge will be extremely important for researchers to develop new treatments and improve clinical outcomes for liver cancer therapy. Liver cancer is difficult to treat and is resistant to the latest immunotherapy. An important reason is that liver cancer tumors are enriched with macrophages. These macrophages suppress immune responses and stop the immune system from clearing the cancer cells. We plan to study an enzyme called KDM1A in tumor macrophages. When this enzyme is absent from the macrophages, they become more inflamed. We want to test whether macrophages lacking KDM1A will help alleviate liver cancer progression and strengthen immunotherapy. We also want to test a new substance that can break down KDM1A. We want to see if this new compound can treat liver cancer. With this project, we hope to find out if removing an epigenetic enzyme called KDM1A in the macrophages will help our immune system fight liver cancer. We also want to evaluate the potential therapeutic effects of a new compound that can degrade KDM1A. We want to find out if this compound can be a good drug for the treatment of liver cancer.
  • Swedish Research Council
    1 January 2024 - 31 December 2026
    Over-nutrition and inflammation induce transcriptional alterations linked with non-alcoholic fatty liver diseases (NAFLD). Such pathological changes are tightly controlled by chromatin remodeling events, particularly at non-coding genomic regions in the liver cells. Those tissue-specific regions are enriched with SNPs but their function and regulation remain largely unknown. The widely used strategies to map active chromatin landscape with epigenetic markers, which have not even been widely applied to human cohorts, are questioned most recently. Studies by us and others have shown that genomic regions featured with active epigenetic markers, and previously clustered as ‘super enhancers’, are not always functionally identical. Many of them are either inactive or repressive (silencers). The molecular traits to differentiate the ‘true’ functional enhancers and silencers are unknown, which halts the efforts for deciphering the true roles of genetic risk factors in NAFLD.The OBJECTIVE of my proposal is to characterize NAFLD/NASH-relevant functional epigenetics and to test proof-of-concept enhancer targeting treatment strategies. We plan to combine molecular techniques and human cohorts to achieve three major AIMs: To identify monocyte and liver epigenetic signatures in NAFLD/NASH cohort.To investigate the functionality of the epigenetic regions in human liver cells.To therapeutically target liver enhancers using tissue-specific oligonucleotides.
  • From epigenetics to functional epigenetics: investigating enhancers and silencers in human metabolic tissues
    Novo Nordisk Foundation
    1 January 2022 - 31 December 2026
  • Swedish Cancer Society
    1 January 2021
    Obesity increases both the risk and mortality of liver cancer. The development of obesity-induced liver cancer is usually initiated with lipid accumulation in the liver and is followed by liver inflammation, liver fibrosis, cirrhosis and then cancer. It is unclear how this process unfolds at the molecular level. Recent advances in DNA technology enable deep investigation of disease progression at the chromatin level. We therefore plan to investigate chromatin regulatory events in both liver hepatocytes and macrophages to understand the driving mechanisms for causing liver cancer in obesity. This study investigates the molecular mechanisms of how obesity triggers liver cancer. It is now clear that both liver lipid dysregulation and liver inflammation contribute to the development of the disease. We therefore plan to investigate the chromatin remodeling events that define progression during NAFLD liver cancer transformation in the hope of identifying novel mechanisms involved in disease progression. We expect to explain how obesity drives liver cancer at the deep-rooted DNA level, which is required to develop intervention strategies. We hope to validate the function of the many NASH fibrosis-related candidates we have identified so far through data mining in human liver disease patients in mouse models. We will continue to explore the new candidates, both drug-targeted proteins and disease-relevant chromatin regions associated with NAFLD liver cancer development using high-throughput objective screening techniques. With all these efforts, we hope to identify major mechanisms that drive the obesity and liver cancer process, which is valuable for understanding the disease for both diagnosis and drug development.
  • Swedish Research Council
    1 January 2020 - 31 December 2023
  • Epigenomic medicine in type 2 diabetes and atherosclerosis: targeting macrophage enhancers
    Novo Nordisk Foundation
    1 January 2020 - 31 December 2022

Employments

  • Principal Researcher, Department of Medicine, Huddinge, Karolinska Institutet, 2024-

Degrees and Education

  • Docent, Karolinska Institutet, 2022

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