Your browser doesn't support javascript.
loading
Endothelial TRPV4 channels in lung edema and injury.
Sonkusare, Swapnil K; Laubach, Victor E.
Afiliación
  • Sonkusare SK; Robert M. Berne Cardiovascular Research Center, University of Virginia, Charlottesville, VA, United States; Department of Molecular Physiology and Biological Physics, University of Virginia, Charlottesville, VA, United States. Electronic address: swapnil.sonkusare@virginia.edu.
  • Laubach VE; Department of Surgery, University of Virginia, Charlottesville, VA, United States.
Curr Top Membr ; 89: 43-62, 2022.
Article en En | MEDLINE | ID: mdl-36210151
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.
Asunto(s)
Palabras clave

Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Edema Pulmonar / Lesión Pulmonar Tipo de estudio: Etiology_studies / Prognostic_studies Límite: Animals Idioma: En Revista: Curr Top Membr Año: 2022 Tipo del documento: Article

Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Edema Pulmonar / Lesión Pulmonar Tipo de estudio: Etiology_studies / Prognostic_studies Límite: Animals Idioma: En Revista: Curr Top Membr Año: 2022 Tipo del documento: Article