Teachings from COVID-19 and aging-An oxidative process

Abstract

As of June 2020, the COVID-19 pandemic has totaled over 9 000 000 cases and 470 000 deaths globally (ref. 1). Emerging data from COVID-19 patients have suggested a clear role for oxidative stress in the pathogenesis of SARS-CoV-2, the pathogenic agent of COVID-19. Several comorbidities, including hypertension, diabetes, obesity, and aging, have been associated with an increase in baseline oxidative stress, likely explaining why such individuals at risk for poor outcomes with SARS-CoV-2 infection. Similarly, the concept of oxidative stress remains one of the best supported theories to explain the mechanism behind aging. Oxidative stress through both endogenous and exogenous sources has known deleterious effects in both aging and SARS-CoV-2 infection. Herein, we will review the role of oxidative stress as a key player in both aging and COVID-19 and highlight why some individuals may have better or poorer outcomes because of this. Additionally, we will discuss potential therapeutic pathways for effectively anti-aging as we take away from our learnings on COVID-19.

Keywords: COVID-19; aging; anti-aging; oxidative stress; skin aging.

FIGURE 1

Oxidative stress. Oxidative stress is thought to play a role in both aging and COVID‐19 pathogenesis. There are both endogenous and exogenous sources of oxidative stress; one of the former is believed to be ANG2. ACE2 degrades ANG2 (a vasoconstrictor and inducer of inflammation) to ANG1/7, which helps counterbalance the effects of ANG2‐induced oxidative stress. SARS‐CoV 2, the pathogenic agent of COVID‐19, enters cells through binding and subsequently downregulating ACE2, resulting in increased ANG2‐induced inflammation. Aging and several comorbidities that have been linked to more severe cases of COVID‐19 are also thought to represent states of ACE2 deficiency (and increased ANG2 levels). ACE2, Angiotensin‐converting enzyme 2; ANG2, Angiotensin 2; ANG1/7, Angiotensin 1 and Angiotensin 7; HTN, Hypertension; CVD; Cardiovascular disease; DM, Diabetes mellitus; ROS, Reactive oxygen species; NADPH oxidase, nicotinamide adenine dinucleotide phosphate oxidase; MPO, myeloperoxidase; LOX, lipoxygenase. Note: Figure adapted from figure in Ref