COVID-19 in the heart and the lungs: could we "Notch" the inflammatory storm?

Basic Res Cardiol. 2020 Apr 9;115(3):31. doi: 10.1007/s00395-020-0791-5.

Abstract

From January 2020, coronavirus disease (COVID-19) originated in China has spread around the world. The disease is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The presence of myocarditis, cardiac arrest, and acute heart failure in COVID-19 patients suggests the existence of a relationship between SARS-CoV-2 infection and cardiac disease. The Notch signalling is a major regulator of cardiovascular function and it is also implicated in several biological processes mediating viral infections. In this report we discuss the possibility to target Notch signalling to prevent SARS-CoV-2 infection and interfere with the progression of COVID-19- associated heart and lungs disease.

Keywords: ADAM17; Angiotensin-converting enzyme 2; COVID-19; Cardiovascular disease; Coronavirus disease; Furin; Notch.

Publication types

  • Editorial

MeSH terms

  • ADAM17 Protein / antagonists & inhibitors
  • Angiotensin-Converting Enzyme 2
  • Betacoronavirus / drug effects
  • Betacoronavirus / pathogenicity*
  • COVID-19
  • China
  • Coronavirus Infections / drug therapy*
  • Coronavirus Infections / pathology
  • Coronavirus Infections / physiopathology*
  • Coronavirus Infections / virology
  • Disease Progression
  • Furin / metabolism
  • Heart Arrest / etiology
  • Heart Arrest / pathology
  • Heart Diseases / drug therapy*
  • Heart Diseases / etiology*
  • Heart Diseases / pathology
  • Heart Diseases / physiopathology
  • Heart Failure / etiology
  • Heart Failure / pathology
  • Humans
  • Interleukin-6 / immunology
  • Lung Diseases / drug therapy*
  • Lung Diseases / etiology*
  • Lung Diseases / pathology
  • Lung Diseases / physiopathology
  • Myocarditis / etiology
  • Myocarditis / pathology
  • Pandemics
  • Peptidyl-Dipeptidase A / deficiency
  • Peptidyl-Dipeptidase A / metabolism
  • Pneumonia, Viral / drug therapy*
  • Pneumonia, Viral / pathology
  • Pneumonia, Viral / physiopathology*
  • Pneumonia, Viral / virology
  • Receptors, Notch / antagonists & inhibitors*
  • Receptors, Notch / metabolism
  • SARS-CoV-2
  • Signal Transduction / drug effects

Substances

  • Interleukin-6
  • Receptors, Notch
  • Peptidyl-Dipeptidase A
  • ACE2 protein, human
  • Angiotensin-Converting Enzyme 2
  • Furin
  • ADAM17 Protein
  • ADAM17 protein, human