There is still much to learn about the SARS-CoV-2 virus that causes COVID-19. For instance, although it infests host cells through ACE2, how the virus impacts the renin-angiotensin-aldosterone system (RAAS) and vice versa is not known. In an article published ahead-of-print, Leo Buckley, Judy Cheng, and Akshay Desai provide an overview of the role of ACE2 in cardiovascular physiology and SARS-CoV-2 virology. Their article (Cardiovascular Pharmacology in the Time of COVID-19: A Focus on Angiotensin Converting Enzyme 2) also tackles the question of how do you manage patients on RAAS inhibitor therapy who have, or are at risk for developing, COVID-19.
The May issue also kicks off a two part invited review series hosted by Robert Lukowski on cGMP/PKGI signaling in the heart (see the accompanying editorial). This axis acts as a counterweight to the sympathetic system and RAAS with antihypertrophic and antifibrotic actions in the heart, as well as offering protection from ischemia and reperfusion injury and cell death. Yet harnessing the cardiac protective potential of the associated pathway(s) in different cell types has mostly proven to be elusive. Altogether 7 articles in the series discuss what is currently known about cGMP/PKGI signaling in the heart and highlight the pressing issues that still wait to be resolved.
