Erbay Laboratory

Atherosclerosis is the leading cause of death in the Western world. Dyslipidemia, obesity and diabetes significantly increase cardiovascular disease (CVD) risk. Other than health style changes, managing diabetes and lowering bad cholesterol, there has been no major breakthrough in the treatment of atherosclerosis in the past two decades. There is a big and unmet need to better understand the molecular mechanisms that drive atherosclerosis progression and its complications through research and to identify new therapeutic targets based on these mechanisms. Studies have shown reducing sterile inflammation that occurs with hyperlipidemia is a particularly promising approach to circumvent the consequences of atherosclerosis in mouse models and humans. Inside the cells, organelles like the endoplasmic reticulum (ER) and mitochondria serve as the centers for the integration of metabolism and immune responses. The major scientific and translational goal of the Erbay Laboratory is to understand organelle stress responses to nutrient excess and in relation to chronic inflammation that drives atherosclerosis progression. We previously showed that small molecule inhibitors and bioactive lipids can modulate ER's stress response to hyperlipidemia and prevent inflammation and atherosclerosis in mouse models. We are currently working on novel molecular as well as metabolite players that can communicate ER stress to other intracellular organelles such as mitochondria and nucleus. In our ongoing studies, we are investigating the contribution of these novel stress communicators in propagating metabolic inflammation and atherosclerosis.

The Erbay Laboratory is affiliated with the Smidt Heart Institute, Department of Cardiology, and Department of Biomedical Sciences.