TRPM7 deficiency exacerbates cardiovascular and renal damage induced by aldosterone-salt.

ABSTRACT: Hyperaldosteronism causes cardiovascular disease as well as hypomagnesemia. Mechanisms are ill-defined but dysregulation of TRPM7, a Mg²⁺-permeable channel/α-kinase, may be important. We examined the role of TRPM7 in aldosterone-dependent cardiovascular and renal injury by studying aldosterone-salt treated TRPM7-deficient (TRPM7^+/Δkinase) mice. Plasma/tissue [Mg²⁺] and TRPM7 phosphorylation were reduced in vehicle-treated TRPM7^+/Δkinase mice, effects recapitulated in aldosterone-salt-treated wild-type mice. Aldosterone-salt treatment exaggerated vascular dysfunction and amplified cardiovascular and renal fibrosis, with associated increased blood pressure in TRPM7^+/Δkinase mice. Tissue expression of Mg²⁺-regulated phosphatase

SUBMITTER: Rios FJ 

PROVIDER: S-EPMC9325869 | biostudies-literature | 2022 Jul

REPOSITORIES: biostudies-literature