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.
I received my MD degree from Ankara University and PhD in cell and structural biology from the University of Illinois, Urbana-Champaign. I have been working on cellular adaptation to nutrient stress since my doctoral studies, which focused on mTOR signaling. My postdoctoral studies with Gökhan S. Hotamışlıgil at the Harvard School of Public Health demonstrated the causality of endoplasmic reticulum (ER) stress to hyperlipidemia-induced inflammation and atherosclerosis. Studies published from my lab further demonstrated that highly specific, small molecule modulators of ER's stress responses can reduce atherosclerosis progression. We are a highly collaborative group that works with experts in diverse fields and utilizes the state-of-the-art research technologies to uncover ER's contribution to cellular homeostasis and stress, with a specific focus on immune cells and in cardiovascular syndrome.
Ebru Erbay, MD, PhD
Collaborations & Resources
Reagents and Resources
- Loss of function mouse models for core proteins in the Unfolded Protein Response
Meet Our Team
Our team is composed of a bright, motivated, dedicated team of international PhD students and postdoctoral fellows representing three continents.
We are always looking for talented and motivated researchers to join our team. For more information, please contact Ebru Erbay, MD directly at firstname.lastname@example.org.
Ona UI, Yildirim AD, Tufanli O, Cimen I, Kocaturk B, Hamid SM, Chen S, Sin J, Shimada K, Shah PK, Gottlieb RA, Arditi M, Erbay E.
J Am Coll Cardiol. 2019 Mar 19;73(10):1149-1169.
Tufanli O, Telkoparan-Akillilar P, Acosta-Alvear D, Kocaturk B, Cimen I, Onat UI, Hamid SM, Walter P, Weber C, Erbay E.
Proc Natl Acad Sci USA. 2017 Feb 21;114(8):E1395-E1404.
Çimen I, Kocatürk B, Koyuncu S, Apaydın O, Tufanlı Ö, Onat UI, Demirsoy Ş, Aykut GZ, Nguyen UT, Watkins SM, Hotamışlıgil GS, Erbay E.
Sci Transl Med. 2016 Sep 28;8(358):358ra126.
Erbay E, Babev VR, Mayers JR, Makowski L, Tape KN, Fazio S, Wiest MM, Watkins SM, Linton MF, Hotamisligil GS.
Nat Med. 2009 Dec;15(12):1383-1391.
Contact the Erbay Lab
If you have any questions or would like more information about the research work at the Erbay Laboratory, please give us a call.
Advanced Health Sciences Pavilion, Room A9104
127 S. San Vicente Blvd.
Los Angeles, CA 90048