Related Experiment Video

Updated: Sep 6, 2025

Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
11:00

Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes

Published on: September 18, 2017

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Direct mechanisms of SARS-CoV-2-induced cardiomyocyte damage: an update

Yicheng Yang1, Zhiyao Wei2, Changming Xiong3,4

  • 1Center for Pulmonary Vascular Diseases, Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Diseases of China, State Key Laboratory of Cardiovascular, Beijing, 100037, China.

Virology Journal
|June 25, 2022
PubMed

Insights

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) directly injures heart muscle cells (cardiomyocytes). This viral invasion impacts heart function and contributes to COVID-19 severity.

Area of Science:

  • Cardiology
  • Virology
  • Pathology

Background:

  • Myocardial injury is linked to severe COVID-19 outcomes.
  • The direct role of SARS-CoV-2 in cardiomyocyte damage requires further elucidation.

Purpose of the Study:

  • To review the direct mechanisms by which SARS-CoV-2 causes myocardial injury.
  • To comprehensively understand the cardiac manifestations of COVID-19.

Main Methods:

  • Review of recent studies on SARS-CoV-2 infection of cardiomyocytes.
  • Analysis of viral entry pathways and downstream effects on cardiac function.

Main Results:

  • SARS-CoV-2 can infect cardiomyocytes via endosomal pathways, independent of full S protein priming.
  • Viral infection impairs cardiomyocyte contractile function and causes electrical dysfunction.
  • SARS-CoV-2 disrupts the renin-angiotensin-aldosterone system, contributing to myocardial injury.

Conclusions:

  • Direct viral invasion plays a significant role in SARS-CoV-2-induced myocardial injury.
  • Understanding these mechanisms is crucial for managing cardiac complications in COVID-19.
Keywords:
COVID-19CardiomyocytesMyocardial injurySARS-CoV-2

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