Robert Raffai, PhD

Associate Professor
+1 415 221-4810 ext. 22451

Dr. Raffai's research program focuses on elucidating the interplay between metabolism and inflammation in atherosclerosis cardiovascular disease and heart failure. Through studies of mouse models developed in his laboratory, Dr. Raffai's team uncovered new pathways through which a protein called ApoE participates in suppressing the progression and in enhancing the regression of atherosclerosis. Their discovery linked ApoE metabolism to microRNA-control of immune cell activation and protection from atherosclerosis in mice with hyperlipidemia. The laboratory now explores how apoE expression in macrophages contributes to the regulated release of non-coding RNA including microRNA into exosomes that can be communicated to cells at a distance to influence inflammation and atherosclerosis. The lab also explores the role of apoE in altering the microRNA composition of plasma lipoproteins that can also serve as a source of extracellular communication. A  more recent topic in the lab include to explore how diabetic hyperglycemia alters the biogenesis and regulated release of microRNA in exosomes derived from myeloid cells, and how these exRNA can serve to enhance systemic and vascular inflammation and atherosclerosis. Our goal is to uncover mechanism through which to prevent microRNA dysregulation in myeloid cells of diabetic mice and to infuse exRNA as novel treatments for diabetic atherosclerosis. Dr. Raffai has trained four postdoctoral fellows and numerous college graduate students in the study of lipoprotein metabolism and immune cell regulation of atherosclerosis.

Primary Thematic Area: 
Vascular & Cardiac Biology
Secondary Thematic Area: 
Research Summary: 
Our program explores the impact of metabolic stress on deregulated micro-RNA controlled hematopoiesis and immune cell function in the pathogenesis of atherosclerosis, including through intercellular signaling via exosomes



Hyperpolarized 13 C magnetic resonance evaluation of renal ischemia reperfusion injury in a murine model.

NMR in biomedicine

Baligand C, Qin H, True-Yasaki A, Gordon JW, von Morze C, Santos JD, Wilson DM, Raffai R, Cowley PM, Baker AJ, Kurhanewicz J, Lovett DH, Wang ZJ

An intracellular matrix metalloproteinase-2 isoform induces tubular regulated necrosis: implications for acute kidney injury.

American journal of physiology. Renal physiology

Ceron CS, Baligand C, Joshi S, Wanga S, Cowley PM, Walker JP, Song SH, Mahimkar R, Baker AJ, Raffai RL, Wang ZJ, Lovett DH

Extending gene ontology in the context of extracellular RNA and vesicle communication.

Journal of biomedical semantics

Cheung KH, Keerthikumar S, Roncaglia P, Subramanian SL, Roth ME, Samuel M, Anand S, Gangoda L, Gould S, Alexander R, Galas D, Gerstein MB, Hill AF, Kitchen RR, Lötvall J, Patel T, Procaccini DC, Quesenberry P, Rozowsky J, Raffai RL, Shypitsyna A, Su AI, Théry C, Vickers K, Wauben MH, Mathivanan S, Milosavljevic A, Laurent LC

Immunosuppression With FTY720 Reverses Cardiac Dysfunction in Hypomorphic ApoE Mice Deficient in SR-BI Expression That Survive Myocardial Infarction Caused by Coronary Atherosclerosis.

Journal of cardiovascular pharmacology

Luk FS, Kim RY, Li K, Ching D, Wong DK, Joshi SK, Imhof I, Honbo N, Hoover H, Zhu BQ, Lovett DH, Karliner JS, Raffai RL