Ethan Weiss, MD


Cardiology UCSF Health

CLINICAL INTERESTS: Dr. Ethan Weiss is a cardiologist specializing in general cardiology. His special interests include preventive cardiology, genetics of coronary disease, risk assessment, and heart disease in the young.

RESEARCH INTERESTS: In his research, Dr. Weiss uses genetic models to better understand the mechanism of metabolic disorders such as obesity, fatty liver disease, and diabetes. He also studies the blood clotting system and has interest in identifying novel ways to safely block clots associated with diseases such as heart attack and stroke without causing an increase in bleeding.

M.D., 1996 - School of Medicine, Johns Hopkins University
Clinical Fellowship, - School of Medicine - Cardiology, University of California, San Francisco
  1. Comparing the Keyto App and Device with Weight Watchers' WW App for Weight Loss: Protocol for a Randomized Trial.
  2. Diet Quality and Visceral Adiposity among a Multiethnic Population of Young, Middle, and Older Aged Adults
  3. Billy Idol.
  4. Adipocyte JAK2 mediates spontaneous metabolic liver disease and hepatocellular carcinoma.
  5. Adipocyte JAK2 Regulates Hepatic Insulin Sensitivity Independently of Body Composition, Liver Lipid Content, and Hepatic Insulin Signaling.
  6. Growth hormone receptor antagonism with pegvisomant in insulin resistant non-diabetic men: A phase II pilot study.
  7. Adipocyte JAK2 mediates growth hormone-induced hepatic insulin resistance.
  8. Hepatocyte-Specific Disruption of CD36 Attenuates Fatty Liver and Improves Insulin Sensitivity in HFD-Fed Mice.
  9. Disruption of JAK2 in adipocytes impairs lipolysis and improves fatty liver in mice with elevated GH.
  10. HIV infection is associated with decreased thrombin generation.
  11. Liver-derived IGF-I contributes to GH-dependent increases in lean mass and bone mineral density in mice with comparable levels of circulating GH.
  12. Abrogation of growth hormone secretion rescues fatty liver in mice with hepatocyte-specific deletion of JAK2.
  13. Genetic regulation of platelet receptor expression and function: application in clinical practice and drug development.
  14. Increased thrombosis susceptibility and altered fibrin formation in STAT5-deficient mice.
  15. Sex differences in thrombosis.
  16. Sex differences in thrombosis in mice are mediated by sex-specific growth hormone secretion patterns.
  17. Protection against thrombosis in mice lacking PAR3.
  18. Role of thrombin signalling in platelets in haemostasis and thrombosis.
  19. Protease-activated receptors 1 and 4 are shut off with distinct kinetics after activation by thrombin.
  20. Structure-function analysis of protease-activated receptor 4 tethered ligand peptides. Determinants of specificity and utility in assays of receptor function.
  21. PAR3 is a cofactor for PAR4 activation by thrombin.
  22. Higher prevalence of GPIIIa PlA2 polymorphism in siblings of patients with premature coronary heart disease.
  23. PlA1/A2 polymorphism of platelet glycoprotein IIIa and risk of cardiovascular disease.
  24. Self-expanding metal stent for obstructing adenocarcinoma of the sigmoid.
  25. A polymorphism of a platelet glycoprotein receptor as an inherited risk factor for coronary thrombosis.
  26. A monoclonal antibody (SZ21) specific for platelet GPIIIa distinguishes P1A1 from P1A2.