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Review
. 2021 Mar:51:102168.
doi: 10.1016/j.scr.2021.102168. Epub 2021 Jan 12.

The effects of novel coronavirus (SARS-CoV-2) infection on cardiovascular diseases and cardiopulmonary injuries

Ni Li  1 , Linwen Zhu  2 , Lebo Sun  2 , Guofeng Shao  3
Affiliations
Review

The effects of novel coronavirus (SARS-CoV-2) infection on cardiovascular diseases and cardiopulmonary injuries

Ni Li et al. Stem Cell Res. 2021 Mar.

Abstract

COVID-19 caused by a novel coronavirus named SARS-CoV-2, can elites severe acute respiratory syndrome, severe lung injury, cardiac injury, and even death and became a worldwide pandemic. SARS-CoV-2 infection may result in cardiac injury via several mechanisms, including the expression of angiotensin-converting enzyme 2 (ACE2) receptor and leading to a cytokine storm, can elicit an exaggerated host immune response. This response contributes to multi-organ dysfunction. As an emerging infectious disease, there are limited data on the effects of this infection on patients with underlying cardiovascular comorbidities. In this review, we summarize the early-stage clinical experiences with COVID-19, with particular focus on patients with cardiovascular diseases and cardiopulmonary injuries, and explores potential available evidence regarding the association between COVID-19, and cardiovascular complications.

Keywords: Cardiopulmonary diseases; Mechanism; SARS-CoV-2.

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Conflict of interest statement

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Figures

Fig. 1
Fig. 1
The role of renin-angiotensin system and myocardial injury caused by SARS-CoV-2 affecting ACE2. The combination of SARS-CoV-2 with ACE2 resulted in the decrease of ACE2 expression, the increase of Ang II expression in plasma and myocardium, and the decrease of Ang(1–7) expression. Inflammatory reaction and oxidative stress induced myocardial injury, which led to decreased myocardial contractility and heart failure. MAS angiopoietin 1–7 receptor, ACE:angiotensin-converting enzyme, AT angiotensin II receptor, Angangiotensin.
Fig. 2
Fig. 2
The mechanism of cytokine storm caused by SARS-CoV-2. After human immune cells are infected with SARS-CoV-2, the immune system releases cytokines such as interferons, interleukins, and chemokines. Excessive cytokines bind to receptors on cell membranes and activate the JAK signaling pathway. The JAK signaling pathway activates the downstream STAT signaling pathway. STAT and phosphorylated STAT family members are combined with specific DNA elements in the nucleus after polymerization, and cytokine-related genes are activated. Eventually trigger a cytokine storm. JAK: Janus kinase, STAT: signal transducer and activator of transcription.
See this image and copyright information in PMC

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