Our lab team studies biochemical and molecular mechanisms mediating atherosclerosis, vascular dysfunction, tissue inflammation, monocyte differentiation, metabolic reprogramming and redox biology regulation responsible for hyperhomocysteinemia (HHcy)-related diseases, stroke, chronic kidney disease, metabolic dysfunction-associated steatotic liver disease (MASLD) and Alzheimer's disease.

We investigate the molecular mechanisms that govern mitochondrial transplantation. Our work focuses on uptake, integration, and functional recovery in injured cells and tissues.

We focus on heart and kidney diseases, exploring how these diseases are influenced by metabolism, inflammation and cell damage. One key research area is acute kidney injury (AKI), which affects about 1 in 5 hospitalized patients. She studies how kidney cells lose energy during injury and is exploring a new therapy called mitochondrial transplantation, which uses healthy mitochondria to help kidneys recover. 

We also study aortic valve disease, a common heart condition in older adults. She discovered that platelets could cause damage to heart valves by triggering calcium buildup. Her findings could lead to new treatments that slow down or stop this disease. In addition, her research shows that a high-sugar diet can harm heart health more than fat by changing gut bacteria and causing inflammation. Our work aims to create better ways to treat and prevent heart and kidney diseases using cutting-edge science.

Research in the Khan laboratory focuses on the overarching premise that reactivation of embryonic signaling in the adult or aged heart enhances cardiac repair potential after injury. The neonatal heart is composed of cardiomyocytes and cardiac progenitor cells (CPCs) able to repair injured myocardium. This repair ability is lost in the adult and aged heart, making it vulnerable to the development of disease.  

Our ongoing efforts focus on identifying and reintroducing reparative factors to enhance cardiac progenitor cells and cardiomyocyte-based repair programs. Whether cardiomyocytes (CPCs) from adults can be reversed into an intermediate developmental state remains untested.  

We have identified a unique embryonic microRNA signaling complex and its pro-reparative benefits for the heart. Currently, we are developing in vitro and in vivo techniques that include mouse transgenesis to measure functional changes in CPCs and cardiomyocyte proliferation, survival and metabolism in response to re-introduction of embryonic reparative factors. 

Additionally, we are evaluating whether stem cell-derived exosomes are a useful cell therapy that can improve cell communication and tissue repair. Overall, our major focus is how developmental signaling factors regulate metabolism to affect cardiac health and disease during cardiometabolic stress and chronic kidney disease. 

The Wei laboratory examines the roles of endoplasmic reticulum-associated degradation (ERAD) in regulating multiple processes in the liver, including lipid metabolism, systemic energy homeostasis, hepatocyte hyperproliferation, iron homeostasis, formation of hepatic inclusions and fibrinogen biogenesis. Defects in ERAD contribute to hepatic proteotoxic stress response, inducing numerous pathological conditions.  

We have discovered a new mechanism — ER proteotoxic stress-m6A pathway (ERm6A) — involved in the response to hepatic proteotoxic stress, based on changes in m6A “writer” METTL14-mediated mRNA methylation. The inhibition of global m6A and suppression of mRNA led to chronic liver injury due to ER stress. Also, ubiquitination mediated by the E3 ligase HRD1 directly targets metabolic enzymes and transcription factors such as CREBH for degradation. These processes influence liver metabolism, metabolic dysfunction-associated steatotic liver disease (MASLD) and development of obesity. Importantly, hepatic HRD1 expression is induced in the postprandial condition upon mouse refeeding.  

Our group is studying these hepatic stress responses and those regulated by a second E3 ligase, MARCH6, in the context of changes in metabolism. 

Dr. Wu’s lab explores how hormones — particularly male hormones called androgens — affect women’s health. High levels of androgens, as seen in conditions such as polycystic ovary syndrome (PCOS), can lead to weight gain, liver problems, diabetes and fertility challenges.  We study how these hormones act on different organs, such as the liver, brain and ovaries, and how these organs communicate with each other to control metabolism and reproduction. We use advanced research tools and specially designed mouse models to uncover why high androgen levels cause certain health problems in women.  

Our ultimate goal is to find new ways to prevent and treat these conditions. By understanding how androgens disrupt normal body functions, we hope to develop better therapies that improve the health and quality of life for women affected by PCOS and similar metabolic disorders.  

The Yu Laboratory explores how blood vessels change and how vascular diseases develop, with implications for heart disease, stroke and diabetes. We aim to uncover the cell and protein signals that guide these changes and apply this knowledge to develop better treatments.  

Our research has three main areas:  

1. Studying how cellular stress contributes to diseases like atherosclerosis and diabetes. We focus on a group of proteins called reticulons and their role in plaque buildup and cell death in arteries.  
2. Investigating vascular and heart scarring, known as fibrosis. We examine how a protein group called MAPK phosphatases affects artery disease and heart injury, and we test new drug candidates that may block their harmful effects.  
3. How blood vessels grow under healthy and diseased conditions. We search for signals that control vessel growth and repair, especially in people with metabolic diseases.  

We combine bioinformatics, AI tools, mouse models, cell biology and biochemistry to uncover pathways that may lead to life-saving therapies.