The Renin Angiotensin System: Insights into the Role of ACE2 in Glomerular Injury Including SARS-CoV-2 Infection

TL;DR

This paper explores how ACE2, an enzyme involved in kidney function, may influence glomerular injury and its role in kidney damage during SARS-CoV-2 infection.

Contribution

The paper provides a narrative review highlighting the role of ACE2 in glomerular injury and its connection to SARS-CoV-2 infection.

Findings

ACE2 is expressed in the glomerulus and degrades angiotensin II, which is linked to inflammation and fibrosis.

ACE2 serves as a receptor for SARS-CoV-2, potentially impacting glomerular injury during COVID-19.

The review summarizes current knowledge on ACE2's role in kidney injury and its broader implications.

Abstract

The circulating renin–angiotensin–aldosterone system (RAAS) plays a key role in regulating blood volume and electrolyte levels. While important for the maintenance of intravascular volume systemically, the local activation of tissue RAAS and the generation of angiotensin II contribute to inflammation and fibrosis. In the kidney, angiotensin II plays a key role in the development and progression of glomerular injury. Angiotensin-converting enzyme 2 (ACE2), an enzyme that degrades angiotensin II, is expressed in the glomerulus, focusing attention not only on the complexity of the RAAS but also identifying a potential new determinant of glomerular injury. Accordingly, we performed a narrative review using the search terms ACE2 and glomerulus in PubMed and Google Scholar to summarize the current understanding of the role of ACE2 in glomerular injury. We also discuss the role of ACE2 as a cellular receptor for SARS-CoV-2 and the potential impact of this function on glomerular injury in the setting of COVID-19.

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