Myocyte Specific Upregulation of ACE2 in Cardiovascular Disease: Implications for SARS-CoV-2 mediated myocarditis
Nathan R. Tucker,1,2* Mark Chaffin,1* Kenneth C. Bedi Jr.,3 Irinna Papangeli,4 Amer-Denis Akkad,4 Alessandro Arduini,1 Sikander Hayat,4 Gökcen Eraslan,5 Christoph Muus,5,6 Roby Bhattacharyya,5,7 Christian M. Stegmann,4 Human Cell Atlas Lung Biological Network+, Kenneth B. Margulies,3 Patrick T. Ellinor1,8
- Precision Cardiology Laboratory, The Broad Institute, Cambridge, MA, USA 02142
- Masonic Medical Research Institute, Utica, NY, USA 13501
- Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA 19104
- Precision Cardiology Laboratory, Bayer US LLC, Cambridge, MA, USA 02142
- The Broad Institute of MIT and Harvard, Cambridge, MA, USA 02142
- John A. Paulson School of Engineering and Applied Sciences, Harvard University, Cambridge, MA, USA 02138
- Infectious Diseases Division, Department of Medicine, Massachusetts General Hospital, Boston, MA 02114
- Cardiovascular Research Center, Massachusetts General Hospital, Boston, MA, USA 02114
* These authors contributed equally
+ Members of the Human Cell Atlas Lung Biological Network at provided in the Supplementary Materials
Coronavirus disease 2019 (COVID-19) is a global pandemic caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). SARS-CoV-2 infection occurs predominantly by binding of the viral surface spike protein to the human angiotensin-converting enzyme 2 (ACE2) receptor. Hypertension and preexisting cardiovascular disease are risk factors for morbidity from COVID-19, and it remains uncertain whether the use of angiotensin-converting enzyme inhibitors (ACEis) or angiotensin receptor blockers affects infection and disease. This uncertainty has provoked public statements by the American Heart Association, the Heart Failure Society of America, and the American College of Cardiology advising continuation of these agents in the absence of compelling new data.
