Ace and hearts2/18/2024 The SARS-CoV-2 virus requires ACE2 to infect cells but the precise relationship between ACE2 levels, viral infectivity and severity of infection are not well understood.Įven so, aside from its ability to bind the SARS-CoV-2 virus, ACE2 has protective effects against tissue injury, by mitigating the pathological effects of ANG II. Does the quantity of receptors determine whether someone gets more or less sick? Studies have found that a lack of ACE2 (in mice) is associated with severe tissue injury in the heart, lungs and other tissue types. Some evidence suggests that ACE2 may be higher in patients with hypertension, diabetes and coronary heart disease. ACE2 is present in all people but the quantity can vary among individuals and in different tissues and cells. Does everyone have the same number of ACE2 on their cells? This “decreased braking” likely contributes to injury, especially to the lungs and heart, in COVID-19 patients. Thus, ACE2 action is “inhibited,” removing the brakes from ANG II signaling and making more ANG II available to injure tissues. When the SARS-CoV-2 virus binds to ACE2, it prevents ACE2 from performing its normal function to regulate ANG II signaling. Of greatest relevance to COVID-19, ANG II can increase inflammation and the death of cells in the alveoli which are critical for bringing oxygen into the body these harmful effects of ANG II are reduced by ACE2. ACE2 converts ANG II to other molecules that counteract the effects of ANG II. Figure adapted from NEJM The Conversation, CC BY-SAĪCE2 is a vital element in a biochemical pathway that is critical to regulating processes such as blood pressure, wound healing and inflammation, called the renin-angiotensin-aldosterone system (RAAS) pathway.ĪCE2 helps modulate the many activities of a protein called angiotensin II (ANG II) that increases blood pressure and inflammation, increasing damage to blood vessel linings and various types of tissue injury. Drugs called ARBs block angiotensin II from interacting with its receptor. Drugs called ACE inhibitors inhibit the formation of angiotensin II, which would otherwise interact with the angiotensin type 1 receptor to produce tissue damage and inflammation. The main role of ACE2 is to break down angiotensin II into molecules that counteract angiotensin II’s harmful effects but if the virus occupies the ACE2 ‘receptor’ on the surface of cells, then its role is blunted (red lines). The ACE enzyme converts angiotensin I into angiotensin II. University of California, San Diego provides funding as a member of The Conversation US. Krishna Sriram does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment. In addition, his institution has received grant support from Allergan, Boehringer-Ingelheim, Bristol-Myers Squibb, Cirius, Eli Lilly and Company, Galectin Therapeutics, Galmed Pharmaceuticals, GE, Genfit, Gilead, Intercept, Grail, Janssen, Madrigal Pharmaceuticals, Merck, NGM Biopharmaceuticals, NuSirt, Pfizer, pH Pharma, Prometheus, and Siemens. ![]() Rohit Loomba serves as a consultant or advisory board member for Arrowhead Pharmaceuticals, AstraZeneca, Bird Rock Bio, Boehringer Ingelheim, Bristol-Myer Squibb, Celgene, Cirius, CohBar, Conatus, Eli Lilly, Galmed, Gemphire, Gilead, Glympse bio, GNI, GRI Bio, Intercept, Ionis, Janssen Inc., Merck, Metacrine, Inc., NGM Biopharmaceuticals, Novartis, Novo Nordisk, Pfizer, Prometheus, Sanofi, Siemens, and Viking Therapeutics. Insel has received funding from the National Institutes of Health (NIH), American Heart Association, Pfizer, Bristol Myers Squibb, Merck, and the American Society for Pharmacology and Experimental Therapeutics.ĭr. Professor of Medicine, University of California, San Diego Professor of Pharmacology and Medicine, University of California, San Diego Postdoctoral Fellow, University of California, San Diego
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