Novel insights on the pulmonary vascular consequences of COVID-19

Am J Physiol Lung Cell Mol Physiol. 2020 Aug 1;319(2):L277-L288. doi: 10.1152/ajplung.00195.2020. Epub 2020 Jun 17.


In the last few months, the number of cases of a new coronavirus-related disease (COVID-19) rose exponentially, reaching the status of a pandemic. Interestingly, early imaging studies documented that pulmonary vascular thickening was specifically associated with COVID-19 pneumonia, implying a potential tropism of the virus for the pulmonary vasculature. Moreover, SARS-CoV-2 infection is associated with inflammation, hypoxia, oxidative stress, mitochondrial dysfunction, DNA damage, and lung coagulopathy promoting endothelial dysfunction and microthrombosis. These features are strikingly similar to what is seen in pulmonary vascular diseases. Although the consequences of COVID-19 on the pulmonary circulation remain to be explored, several viruses have been previously thought to be involved in the development of pulmonary vascular diseases. Patients with preexisting pulmonary vascular diseases also appear at increased risk of morbidity and mortality. The present article reviews the molecular factors shared by coronavirus infection and pulmonary vasculature defects, and the clinical relevance of pulmonary vascular alterations in the context of COVID-19.

Keywords: COVID-19; SARS-CoV-1; SARS-CoV-2; coronavirus; pulmonary vascular diseases; vascular remodeling.

Publication types

  • Review

MeSH terms

  • Angiotensin-Converting Enzyme 2
  • Betacoronavirus* / pathogenicity
  • Betacoronavirus* / physiology
  • COVID-19
  • Coronavirus Infections / complications*
  • Coronavirus Infections / physiopathology
  • Coronavirus Infections / virology
  • Cytokines / blood
  • DNA Damage
  • Heart Injuries / etiology
  • Host Microbial Interactions / physiology
  • Humans
  • Hypoxia / etiology
  • Inflammation Mediators / blood
  • Lung / blood supply*
  • Lung / physiopathology*
  • Lung / virology
  • Lung Diseases / etiology*
  • Lung Diseases / physiopathology
  • Lung Diseases / virology
  • Mitochondria / physiology
  • Myocardium
  • Oxidative Stress
  • Pandemics
  • Peptidyl-Dipeptidase A / physiology
  • Pneumonia, Viral / complications*
  • Pneumonia, Viral / physiopathology
  • Pneumonia, Viral / virology
  • Pulmonary Circulation
  • Pulmonary Embolism / etiology
  • Receptors, Virus / physiology
  • Risk Factors
  • SARS-CoV-2
  • Vasculitis / etiology


  • Cytokines
  • Inflammation Mediators
  • Receptors, Virus
  • Peptidyl-Dipeptidase A
  • ACE2 protein, human
  • Angiotensin-Converting Enzyme 2