Deletion of Endothelial TRPV4 Protects Heart From Pressure Overload-Induced Hypertrophy

Left ventricular hypertrophy is a bipolar response, starting as an adaptive response to the hemodynamic challenge, but over time develops maladaptive pathology partly due to microvascular rarefaction and impaired coronary angiogenesis. Despite the profound influence on cardiac function, the mechanot...

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Veröffentlicht in:	Hypertension (Dallas, Tex. 1979) Tex. 1979), 2023-11, Vol.80 (11), p.2345-2356
Hauptverfasser:	Adapala, Ravi K, Katari, Venkatesh, Kanugula, Anantha K, Ohanyan, Vahagn, Paruchuri, Sailaja, Thodeti, Charles K
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Cardiomegaly - genetics Disease Models, Animal Endothelial Cells - metabolism Humans Hypertrophy, Left Ventricular - metabolism Mechanotransduction, Cellular Mice Mice, Inbred C57BL Mice, Knockout Myocytes, Cardiac - metabolism TRPV Cation Channels - genetics TRPV Cation Channels - metabolism Vascular Endothelial Growth Factor A - metabolism
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