Javier E. Lopez is interested in studying how soluble factors may regulate the transition of cardiac myocytes from regeneration during fetal growth to hypertrophic growth postnatally. It is postulated that the lack of cardiac regeneration in the postnatal heart confounds the myocyte dysfunction, cell death and tissue fibrosis that is associated with decompensated heart failure. Our global hypothesis is that by manipulating the cardiac gene program of the failing heart with soluble factors (drugs), we may augment endogenous and/or transplanted cardiac myocyte regeneration to ameliorate the progression of left and/or right ventricular failure. My laboratory focus is in studying the fundamental mechanisms of this growth transition to enhance the translational efficacy of soluble factors (drugs) and cell-based strategies (stem-cells) for cardiac regeneration in the failing heart.
M.D., Temple University School of Medicine, Philadelphia, Pennsylvania, 1999
University of Texas Southwestern, Parkland Hospital, Dallas, Texas, 2002
UC Davis, Sacramento, California, 2009
UC San Francisco, San Francisco, California, 2006
UC San Francisco, San Francisco, California, 2007
American Board of Internal Medicine, 2002
American Board of Internal Medicine, Cardiovascular Medicine, 2010
Alpha Omega Alpha
Fellow and Scholar, Sarnoff Endowment for Cardiovascular Research
Member, American Heart Association, Basic Science Council
Member, International Society for Stem Cell Research
Select Recent Publications
Sirish P, Li N, Liu J, Lee K, Hwang SH, Qiu H, Ma S, L?pez JE, Hammock BD, Chiamvimonvat N: Unique Mechanistic Insights into the Beneficial Effects of Soluble Epoxide Hydrolase Inhibitors in the Prevention of Cardiac Fibrosis. Proc Natl Acad Sci U S A, 2013
Watt C, Sirish P, Chiamvimonvat N, López JE: MicroRNAs as a window into cellular processes occurring soon after acute myocardial infarction. World Congress of Heart Disease (Abstract) 2012.
Lopez JE, Myagmar BE, Swigart PM, Montgomery MD, Haynam S, Bigos M, Rodrigo M, Simpson PC. Beta-Myosin Heavy Chain Is Induced by Pressure Overload in a Minor Sub-Population of Smaller Mouse Cardiac Myocytes. Circulation Research. 2011, 109:629-638.
Sirish P, L?pez JE, Li N, Wong A, Timofeyev V, Young JN, Majdi M, Li RA, Chen HS, Chiamvimonvat N. (2012). MicroRNA profiling predicts a variance in the proliferative potential of cardiac progenitor cells derived from neonatal and adult murine hearts. J Mol Cell Cardiol. Jan;52(1):264-72. Epub 2011 Oct 20.
Timofeyev V, Porter CA, Tuteja D, Qiu H, Li N, Tang T, Singapuri A, Han PL, Lopez JE, Hammond KH, and Chiamvimonvat N. Disruption of Adenylyl Cyclase Type V does not Rescue the Phenotype of Cardiac-Specific Over-Expression of Gaq Protein-Induced Cardiomyopathy. American Journal of Physiology. 2010, 299(5):H1459-67.
Lopez JE, Yeo K, Caputo G, Buonocore MH and Schaefer S. Recovery of methamphetamine-associated cardiomyopathy using late gadolinium contrast enhanced magnetic resonance imaging: case report. 2009. Journal of cardiovascular MR. 11:46.
Epting CL*, Lopez JE*, Pendersen A, Brown C, Spitz P, Ursell PC, and Bernstein HS. Stem cell antigen-1 regulates the tempo of muscle repair through effects on proliferation of a7 integrin-expressing myoblasts. 2008. Experimental Cell Research. 314: 1125-1135. 2008. *co-authors listed alphabetically.
Lopez JE, Myagmar BE, Swigart P, Bigos M, Rodrigo M, Simpson PC. Beta-Myosin Heavy Chain induction after pressure overload is in a minor sub-population of myocytes and requires the Alpha-1A-Adrenergic Receptor. 2007. Circulation Supplement. 116(II) 19. Abstract.
Epting CL, Lopez JE, Shen X, Liu L, Bristow J, and Bernstein HS. Stem cell antigen-1 is necessary for cell-cycle withdrawal and myoblast differentiation in C2C12 cells. 2004. Journal of Cell Science. 117(25): 6185-6195.