Ablation of Slc26a6 Mitigates Myocardial Ischemia/Reperfusion Injury.

ABSTRACT: Background/Objectives: Ischemic heart disease remains a leading cause of morbidity and mortality worldwide, accompanied by a major decline in local myocardial pH. However, the mechanisms of pH regulation and the homeostasis of H⁺ neutralizing buffers, such as HCO₃^-, in cardiomyocytes remain incompletely understood. We identified a solute carrier, Slc26a6, in mouse and human hearts playing key roles in the regulation of cardiac pH, excitability, and contractility. Slc26a6 is an acid loader, so we hypothesized that ablation of Slc26a6 may protect the heart from ischemia/reperfusion (I/R) injury. Methods: The I/R model was generated using wild type (WT) and Slc26a6 knockout (Slc26a6^-/-) mice. Multidisciplinary in vivo, in vitro,

SUBMITTER: Thai PN 

PROVIDER: S-EPMC12730430 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature