Type 2 alveolar epithelial cell-derived circulating extracellular vesicle-encapsulated surfactant protein C as a mediator of cardiac inflammation in COVID-19

Inflamm Res. 2022 Sep;71(9):1003-1009. doi: 10.1007/s00011-022-01612-z. Epub 2022 Jul 31.

Abstract

Among the countless endeavours made at elucidating the pathogenesis of COVID-19, those aimed at the histopathological alterations of type 2 alveolar epithelial cells (AT2) are of outstanding relevance to the field of lung physiology, as they are the building blocks of the pulmonary alveoli. A merit of high regenerative and proliferative capacity, exocytotic activity resulting in the release of extracellular vesicles (EVs) is particularly high in AT2 cells, especially in those infected with SARS-CoV-2. These AT2 cell-derived EVs, containing the genetic material of the virus, might enter the bloodstream and make their way into the cardiovascular system, where they may infect cardiomyocytes and bring about a series of events leading to heart failure. As surfactant protein C, a marker of AT2 cell activity and a constituent of the lung surfactant complex, occurs abundantly inside the AT2-derived EVs released during the inflammatory stage of COVID-19, it could potentially be used as a biomarker for predicting impending heart failure in those patients with a history of cardiovascular disease.

Keywords: COVID-19; Cardiac inflammation; Extracellular vesicle; Surfactant protein C; Type 2 alveolar epithelial cell.

Publication types

  • Letter

MeSH terms

  • Alveolar Epithelial Cells
  • COVID-19*
  • Cells, Cultured
  • Extracellular Vesicles*
  • Heart Failure*
  • Humans
  • Inflammation
  • Protein C
  • SARS-CoV-2
  • Surface-Active Agents

Substances

  • Protein C
  • Surface-Active Agents