- University of Texas MD Anderson Cancer Center
The primary goal of our laboratory is to understand the molecular mechanisms of atherosclerosis formation and heart failure as driven by shear stress, diabetes, and specific cancer therapies. These efforts led us to focus on the roles of oxidative stress in regulating post-translational modifications during the process of cardiovascular disease. In particular, we have defined the molecular mechanisms of p90RSK-mediated ERK5 phosphorylation during the development of atherosclerosis as well as heart failure after ischemia/reperfusion injury. Furthermore, we discovered the crucial role of SUMOylation in disturbed flow-induced endothelial activation. In HIV+ patients, cardiovascular disease (CVD) is the third most frequent non-AIDS cause of death, and is the leading cause of death in those received combination antiretroviral therapy (cART). Similarly, CVD is the second leading cause of premature morbidity and mortality among breast cancer, Hodgkin or non-Hodgkin lymphoma, and lung cancer survivors more than 5 years after their diagnosis and treatment. We are now investigating how telomere dysfunction and mitochondrial dysfunction induced by cART and chemo-radiation can coordinately regulate senescence-associated secretory phenotype (or stemness), and develop cardiovascular diseases, particularly in HIV+ and cancer survivors.
|Sep. 9 (Wed)
||Stress-Induced Premature Aging Mediated by Mitochondrial Hibernation Promotes Atherosclerosis