Rajan Sah, MD, PhD

Contact Information

Office: 4334 PBDB
Phone: 319-353-5660
Faculty Profile

Brief description of current research:

Obesity, diabetes and metabolic syndrome are major public health problems and significant risk factors for heart disease in the United States and world-wide. As a clinical cardiologist, I am faced with managing these conditions in patients on a regular basis. My lab is currently focused on studying ion channels as regulators of cellular metabolism in skeletal muscle, adipose tissue and myocardium. Specifically, my research interests focus on intracellular signaling of transient receptor potential channels (including TRPV3, TRPV4 and TRPM7), and the recently identified volume regulatory anion channel SWELL1 (LRRC8a) as they relate to obesity and metabolism. To do this we combine cellular electrophysiology, calcium imaging (GCaMP6) and novel genetic techniques (including transient and stable lenti/AAV-shRNA-mediated knockdown and CRISPR/cas9-mediated knockout) in cultured cells (mouse and human) and freshly isolated primary cells (adipocytes, skeletal muscle fibers, cardiomyocytes). Genetic loss-of-function (CRISPR/cas9-mediated and conventional) mouse models for these ion channels are also used to examine the contributions of these ion channels in vivo and in disease settings. Through a close collaboration with the bariatric surgery program we also have access to freshly isolated human adipocytes from obese and lean patients for acute electrophysiological experiments and long-term culture.

3 most influential diabetes/obesity/metabolism 

  • Ye L, Kleiner S, Wu J, Sah R, Gupta RK, Banks AS, Cohen P, Khandekar MJ, Boström P, Mepani RJ, Laznik D, Kamenecka TM, Song X, Liedtke W, Mootha VK, Puigserver   P, Griffin PR, Clapham DE, Spiegelman BM.  TRPV4 is a regulator of adipose oxidative metabolism, inflammation, and energy homeostasis.  Cell 2012; 151(1):96-110. PMC3477522
  • Sah R, Mesirca P, Mason X, Gibson W, Bates-Withers C, Van den Boogert M, Chaudhuri D, Pu WT, Mangoni ME, Clapham DE.  Timing of myocardial trpm7 deletion during cardiogenesis variably disrupts adult ventricular function, conduction, and repolarization.  Circulation 2013; 128(2):101-114. PMC3800036
  • Sah R, Mesirca P, Van den Boogert M, Rosen J, Mably J, Mangoni ME, Clapham DE.  Ion channel-kinase TRPM7 is required for maintaining cardiac automaticity. Proc Natl Acad Sci USA. 2013; 110(32):E3037-3046.  PMC3740880.


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