Education:
07/1995 B.S in Microbiology, Nanjing Agricultural University, Nanjing, China
07/1999 M.S in Microbiology, China Agricultural University, Beijing, China
05/2005 Ph. D in Molecular Genetics, Michigan State University, East Lansing, MI, USA
06/2010 Postdoctoral Fellow in Endocrinology and Metabolism, Baylor College of Medicine, Houston, TX
Clinical/Research Interests:
The research in my laboratory primarily focuses on understanding the mechanisms that regulate nutrient and energy metabolism, and how they become reprogrammed in obesity, lipodystrophy, and cardiometabolic diseases. We are specifically interested in the following areas: (1) Adipose biology and energy balance in obesity and lipodystrophy; (2) Cardiac substrate utilization in heart failure; (3) Lipid metabolism in liver pathophysiology. Using in vitro molecular/cellular biology approaches, a combination of genomics, transcriptomics, proteomics, CRISP/Cas9-mediated genome editing, and state-of-the-art in vivo mouse physiology analyses, we aim to define the pathological alterations of metabolic communication in diseases including obesity, diabetes, and their associated liver and heart diseases. Ultimately, we aim to identify targets and design therapeutics for these diseases.
1. Adipose tissue development in obesity and lipodystrophy.
Obesity is a global epidemic with serious health and economic burdens. Adipose tissue acts as an endocrine organ, crucial in obesity and metabolic disorders. White adipocytes store triglycerides, while brown and beige adipocytes produce heat through nonshivering thermogenesis, essential for energy balance. We developed lipodystrophic Bscl2 knockout mice, revealing its role in adipose maintenance and associated health issues. Our research focuses on molecular functions of posttranslational modifications and GWAS-identified genes in adipose development, obesity, and lipodystrophy.
2. Lipid metabolism in metabolic cardiomyopathy.
Metabolic disruptions underlie many cardiomyopathies. In healthy humans, fatty acid oxidation supplies 60-70% of myocardial energy. In obesity and diabetes, increased FA supply raises FA oxidation, reducing efficiency and causing lipotoxicity. Heart triglycerides (TGs) provide FAs and regulate heart function. We showed BSCL2's essential role in cardiac substrate use and function. We aim to better understand the mechanisms of cardiac TG lipolysis, mitochondrial function, and metabolic cardiomyopathy.
3. Liver pathophysiology in obesity and diabetes.
Metabolic dysfunction-associated steatotic liver disease (MASLD) spans from simple fat accumulation in the liver to Metabolic Dysfunction-Associated Steatohepatitis (MASH), which involves inflammation and increasing fibrosis, possibly resulting in cirrhosis and liver failure. MASLD affects up to 70% of individuals with T2D. Those with diabetes are at significantly higher risk of developing MASH, cirrhosis, and hepatocellular carcinoma. Current treatment options are limited due to a poor understanding of the molecular processes behind MASLD and MASH. Our research highlights the crucial role of NAE1-mediated neddylation in liver development and function. We aim to identify new factors that contribute to liver diseases in obesity and diabetes.
Funding:
04/01/2016-05/31/2028, Chen, Weiqin (PI) $547,991/year, 2R01HL132182-06A1 National Heart, Lung and Blood Institute, “Novel Role of Bscl2 in Cardiac Substrate Metabolism and Function”
05/01/2024-4/30/2028, Chen, Weiqin (PI) $445,060/year, R01DK135657A1, National Institute of Diabetes and Digestive and Kidney Diseases, “Novel Posttranslational Modifications in Adipose Biology”
01/01/2026-12/31/2027, Shayantani Chakraborty (PI) Chen, Weiqin (Mentor) 77,852/year, 26POST1561360, American Heart Association, “Novel role of TAMM41 in adipose tissue development and obesity”
Select Honors and Accomplishments:
2026-present, Chair of Awards Committee, Endocrinology and Metabolism Section, American Physiological Society
2023-2026, Committee-on-Committees Representative, Endocrinology and Metabolism Section, American Physiological Society
11/2025, Session moderator, “Endocrine Mechanisms that Regulate Cardiometabolic Health” AHA Scientific Session, New Orleans, LA
04/2025, Session moderator, “The Impact of Diet on Metabolic Health and Disease” APS Summit, Baltimore, MA
2017, Outstanding Young Basic Science Faculty Award from MCG Faculty Senate
2013, RNA-Seq Grant, Augusta University Cancer Center
2013, Eugenia Rosenberg Travel Award, Endocrine Society
2008, Postdoctoral Fellowship, American Heart Association
2006, Mentor-Based Postdoctoral Fellowship, American Diabetes Association
2004, DuVall Award (Excellent graduate student scholarship), Michigan State University
Select Publications:
- Zhou H, Xu C, Lee H, Yoon Y, Chen W*. Berardinelli-Seip Congenital Lipodystrophy 2/Seipin Determines Brown Adipose Tissue Maintenance and Thermogenic Programming. Mol Metab. 2020 Mar 4; 36:100971.
- Zhou H, Li J, Su H, Li J, Lydic TA, Young ME, Chen W*. BSCL2/Seipin Deficiency in Heart Causes Energy Deficit and Heart Failure through Inducing Excessive Lipid Catabolism. Clin Transl Med. 2022 Apr;12(4):e736.
- Xu C, Zhou H, Jin Y, Sahay K, Robicsek A, Liu Y, Dong K, Zhou J, Barrett A, Su H and Chen W*. Neddylation Deficiency in Hepatocytes Triggers Fatal Liver Injury via Inducing NF-κB-inducing Kinase. Nat Commun. 2022 Dec 16;13(1):7782. PMID: 36526632.
- Zhou H, Fick K, Patel V, Hilton R, Kim H-W, Bagi Z, Weintraub NL, Chen W*. AGPAT3 Deficiency Impairs Adipocyte Differentiation and Leads to a Lean Phenotype in Mice. American Journal of Physiology Endocrinology and Metabolism. 2024 Jul 1;327(1):E69-E80.
- Zhou H, Christopher CJ, Jones K, Mendiola PM; Gross R, Campagna SR, Bowles DE, Chen W*. Myocardial Metabolic Remodeling in Human End-Stage Ischemic and Non-Ischemic Cardiomyopathy. J Mol Cell Cardiol. 2026 Feb 26:S0022-2828(26)00032-5. doi: 10.1016/j.yjmcc.2026.02.008.
Link to full publication list: https://www.ncbi.nlm.nih.gov/myncbi/weiqin.chen.1/bibliography/public/