TRPC6 Deficiency Attenuates Mitochondrial and Cardiac Dysfunction in Heart Failure with Preserved Ejection Fraction Induced by High-Fat Diet Plus L-NAME.

ABSTRACT: Transient receptor potential canonical channel type 6 (TRPC6), a non-selective cation channel that mediates Ca²⁺ influx, is expressed in the heart and implicated in pathological cardiac hypertrophy. However, the role of TRPC6 in regulating cardiac mitochondrial metabolism and contributing to development of HFpEF remains unclear. We examined whether TRPC6 deficiency prevents mitochondrial dysfunction and offers cardiac protection in a mouse model of HFpEF induced by high-fat diet (HFD) for 12 weeks combined with L-NAME administration during the final 8 weeks in TRPC6 knockout (KO) and wild-type (WT) control mice. Cardiac systolic and diastolic functions were assessed at baseline, 4 and 8 weeks after HFD+L-NAME. Dobutamine-induced stress test and treadmill exercise test were perfo

SUBMITTER: Li X 

PROVIDER: S-EPMC12524895 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature