Abstract
Since the first cases of atypical pneumonia linked to the Huanan Seafood Wholesale Market in Wuhan, China, were described in late December 2019, the global landscape has changed radically. In March 2020, the World Health Organization declared COVID-19 a global pandemic, and at the time of writing this review, just over three million individuals have been infected with more than 200,000 deaths globally. Numerous countries are in ‘lockdown’, social distancing is the new norm, even the most advanced healthcare systems are under pressure, and a global economic recession seems inevitable. A novel coronavirus (SARS-CoV-2) was identified as the aetiological agent. From experience with previous coronavirus epidemics, namely the severe acute respiratory syndrome (SARS) and Middle East Respiratory Syndrome (MERS) in 2004 and 2012 respectively, it was postulated that the angiotensin-converting enzyme-2 (ACE2) receptor is a possible port of cell entry. ACE2 is part of the renin-angiotensin system and is also associated with lung and cardiovascular disorders and inflammation. Recent studies have confirmed that ACE2 is the port of entry for SARS-CoV-2. Male sex, advanced age and a number of associated comorbidities have been identified as risk factors for infection with COVID-19. Many high-risk COVID-19 patients with comorbidities are on ACE inhibitors and angiotensin receptor blockers, and this has sparked debate about whether to continue these treatment regimes. Attention has also shifted to ACE2 being a target for future therapies or vaccines against COVID-19. In this review, we discuss COVID-19 and its complex relationship with ACE2.
Highlights
In these unprecedented times, the Coronavirus disease 2019 (COVID-19) pandemic has had a severe impact globally
These low angiotensin-converting enzyme-2 (ACE2) concentrations were associated with lung oedema and acute lung injury, which contributed to the severe lung pathology in patients already on angiotensin converting enzyme (ACE) inhibitors at the time of severe acute respiratory syndrome (SARS)-CoV infection
Wang et al found that ACE inhibitors and angiotensin receptor blocker (ARB) offer partial cardiovascular protection by increasing ACE2, and that IV recombinant ACE2 may be beneficial in preventing pulmonary arterial hypertension and acute lung injury.[41]
Summary
The Coronavirus disease 2019 (COVID-19) pandemic has had a severe impact globally. ACE2 expression is increased with the use of PPAR-c agonists.[26] PPAR-c agonists, thiazolidinediones, attenuate the development of hypertension and improve endothelial dysfunction in angiotensin II-infused rats.[43] These rats had decreased AT1 expression; the effects were most likely mediated through AT2 receptor activation.[44] PPAR-c agonists were shown to increase the risk of congestive heart failure and possibly myocardial infarction.
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