Endothelial TRPV4 channels in lung edema and injury

Curr Top Membr. 2022:89:43-62. doi: 10.1016/bs.ctm.2022.07.001. Epub 2022 Jul 28.

Abstract

The alveolo-capillary barrier is relatively impermeable, and facilitates gas exchange via the large alveolar surface in the lung. Disruption of alveolo-capillary barrier leads to accumulation of edema fluid in lung injury. Studies in animal models of various forms of lung injury provide evidence that TRPV4 channels play a critical role in disruption of the alveolo-capillary barrier and pathogenesis of lung injury. TRPV4 channels from capillary endothelial cells, alveolar epithelial cells, and immune cells have been implicated in the pathogenesis of lung injury. Recent studies in endothelium-specific TRPV4 knockout mice point to a central role for endothelial TRPV4 channels in lung injury. In this chapter, we review the findings on the pathological roles of endothelial TRPV4 channels in different forms of lung injury and future directions for further investigation.

Keywords: Alveolo-capillary barrier; Endothelium; Lung injury; Pulmonary edema; TRPV4 channels.

Publication types

  • Review

MeSH terms

  • Animals
  • Calcium / metabolism
  • Endothelial Cells / metabolism
  • Endothelium / metabolism
  • Lung / metabolism
  • Lung Injury* / pathology
  • Mice
  • Mice, Knockout
  • Pulmonary Edema* / etiology
  • Pulmonary Edema* / pathology
  • TRPV Cation Channels

Substances

  • TRPV Cation Channels
  • Trpv4 protein, mouse
  • Calcium