Introduction
Patients with cardiovascular and renal diseases are frequently treated with drugs interfering with the Renin-Angiotensin-Aldosterone (RAAS) System. The clinical benefit of angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) are well established and hence became part of treatment guidelines for these patients worldwide. Angiotensin-converting enzyme 2 (ACE2) is an isoenzyme of angiotensin-converting enzyme 1 (ACE). Both are essential parts of the RAAS, see figure 1. ACE2 is involved in cardiac function, the development of hypertension and diabetes mellitus. Also, ACE2 has been identified as a functional receptor for coronaviruses, including SARS-CoV and SARS-CoV-2. SARS-CoV-2 infection is triggered by the binding of the spike protein of the virus to ACE2. It was suggested that patients with cardiac and renal diseases, hypertension, and diabetes, who are treated with drugs potentially increasing ACE2 expression in the lungs such as ACE inhibitors or angiotensin II receptor blockers are at higher risk for severe COVID-19 infection (Fang, Karakiulakis & Roth, 2020; Zheng, Ma, Zhang & Xie, 2020). In the current review, we are summarizing the molecular evidence for this hypothesis (see figure 1 and supplementary material: Molecular Background), next we present results of a meta-analysis of studies analyzing the effects of RAAS blocking drugs (ACE inhibitors, ARBs) on the risk and mortality of pneumonia in non-COVID-19 patients and also meta-analysed the 17 so far published studies on this topic in COVID-19 patients.