M
Mark C. Chappell
Researcher at Wake Forest University
Publications - 245
Citations - 19611
Mark C. Chappell is an academic researcher from Wake Forest University. The author has contributed to research in topics: Angiotensin II & Renin–angiotensin system. The author has an hindex of 68, co-authored 236 publications receiving 17351 citations. Previous affiliations of Mark C. Chappell include Roy J. and Lucille A. Carver College of Medicine & Cleveland Clinic.
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Journal ArticleDOI
A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus–induced lung injury
Keiji Kuba,Yumiko Imai,Shuan Rao,Hong Gao,Feng Guo,Bin Guan,Yi Huan,Peng Yang,Yanli Zhang,Wei Deng,Linlin Bao,Binlin Zhang,Guang Liu,Zhong Wang,Mark C. Chappell,Yanxin Liu,Dexian Zheng,Andreas Leibbrandt,Teiji Wada,Arthur S. Slutsky,Depei Liu,Chuan Qin,Chengyu Jiang,Josef M. Penninger +23 more
TL;DR: A molecular explanation why SARS-CoV infections cause severe and often lethal lung failure and suggest a rational therapy for SARS and possibly other respiratory disease viruses is provided.
Journal ArticleDOI
Angiotensin-converting enzyme 2 is an essential regulator of heart function
Michael A. Crackower,Renu Sarao,Renu Sarao,Gavin Y. Oudit,Gavin Y. Oudit,Chana Yagil,Ivona Kozieradzki,Ivona Kozieradzki,Sam E. Scanga,Antonio J. Oliveira-dos-Santos,Joan da Costa,Liyong Zhang,York Pei,James W. Scholey,Carlos M. Ferrario,Armen S. Manoukian,Mark C. Chappell,Peter H. Backx,Peter H. Backx,Yoram Yagil,Josef M. Penninger +20 more
TL;DR: These genetic data for ACE2 show that it is an essential regulator of heart function in vivo and targeted disruption of ACE2 in mice results in a severe cardiac contractility defect, increased angiotensin II levels, and upregulation of hypoxia-induced genes in the heart.
Journal ArticleDOI
Effect of angiotensin-converting enzyme inhibition and angiotensin II receptor blockers on cardiac angiotensin-converting enzyme 2.
Carlos M. Ferrario,Jewell A. Jessup,Mark C. Chappell,David B. Averill,K. Bridget Brosnihan,E. Ann Tallant,Debra I. Diz,Patricia E. Gallagher +7 more
TL;DR: Although the predominant effect of ACE inhibition may result from the combined effect of reduced Ang II formation and Ang-(1–7) metabolism, the antihypertensive action of AT1 antagonists may in part be due to increased Ang II metabolism by ACE2.
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COVID-19, ACE2, and the cardiovascular consequences.
TL;DR: The current perspective critically examines the evidence for ACE2 regulation by RAAS blockade and statins, the cardiovascular benefits of ACE2, and whether ACE2 blockade is a viable approach to attenuate COVID-19.
Journal ArticleDOI
Counterregulatory Actions of Angiotensin-(1-7)
TL;DR: The accumulating evidence suggests that Ang-(1-7) may oppose the actions of Ang II either directly or by stimulation of prostaglandins and nitric oxide, which may explain the effective antihypertensive action of converting enzyme inhibitors in a variety of non-renin-dependent models of experimental and genetic hypertension as well as most forms of human hypertension.