Activation of Kir2.1 improves myocardial fibrosis by inhibiting Ca ²⁺ overload and the TGF-β1/Smad signaling pathway.

ABSTRACT: The inwardly rectifying potassium channel Kir2.1 is closely associated with many cardiovascular diseases. However, the effect and mechanism of Kir2.1 in diabetic cardiomyopathy remain unclear. In vivo, we use STZ to establish the model, and ventricular structural changes, myocardial inflammatory infiltration, and myocardial fibrosis severity are detected by echocardiography, histological staining, immunohistochemistry, and western blot analysis, respectively. In vitro, a myocardial fibrosis model is established with high glucose. The Kir2.1 current amplitude, intracellular calcium concentration, fibrosis-related proteins, and TGF-β1/Smad pathway proteins are detected by whole-cell patch clamp, calcium probes, western blot analysis, and immunofluorescence, respectively. The

SUBMITTER: Rong Y 

PROVIDER: S-EPMC10281881 | biostudies-literature | 2023 May

REPOSITORIES: biostudies-literature