SARS-CoV-2 as a Factor to Disbalance the Renin-Angiotensin System: A Suspect in the Case of Exacerbated IL-6 Production.
Rafael FrancoRafael Rivas-SantistebanJoan Serrano-MarínAna Isabel Rodriguez-PerezJosé L Labandeira-GarcíaGemma NavarroPublished in: Journal of immunology (Baltimore, Md. : 1950) (2020)
Fever in infections correlates with inflammation, macrophage infiltration into the affected organ, macrophage activation, and release of cytokines involved in immune response, hematopoiesis, and homeostatic processes. Angiotensin-converting enzyme 2 (ACE2) is the canonical cell surface receptor for SARS-CoV-2. ACE2 together with angiotensin receptor types 1 and 2 and ACE2 are components of the renin-angiotensin system (RAS). Exacerbated production of cytokines, mainly IL-6, points to macrophages as key to understand differential COVID-19 severity. SARS-CoV-2 may modulate macrophage-mediated inflammation events by altering the balance between angiotensin II, which activates angiotensin receptor types 1 and 2, and angiotensin 1-7 and alamandine, which activate MAS proto-oncogene and MAS-related D receptors, respectively. In addition to macrophages, lung cells express RAS components; also, some lung cells are able to produce IL-6. Addressing how SARS-CoV-2 unbalances RAS functionality via ACE2 will help design therapies to attenuate a COVID-19-related cytokine storm.
Keyphrases
- sars cov
- angiotensin converting enzyme
- angiotensin ii
- induced apoptosis
- respiratory syndrome coronavirus
- vascular smooth muscle cells
- oxidative stress
- immune response
- cell surface
- adipose tissue
- cell cycle arrest
- wild type
- coronavirus disease
- binding protein
- endoplasmic reticulum stress
- dendritic cells
- cell death
- signaling pathway
- pi k akt