The SGLT2 inhibitor canagliflozin attenuates mitochondrial oxidative stress and alterations of calcium handling induced by high glucose in human cardiac fibroblasts DOI
Fahimeh Varzideh, Urna Kansakar, Scott Wilson

и другие.

Cell Cycle, Год журнала: 2025, Номер unknown, С. 1 - 8

Опубликована: Апрель 21, 2025

Cardiac fibrosis and remodeling are critical contributors to heart failure, particularly in the context of diabetes, where hyperglycemia (HG) exacerbates pathological fibroblast activity. Despite known cardiovascular benefits canagliflozin (CANA), its specific effects on human cardiac fibroblasts (HCFs) under HG conditions remain unexplored. We investigated whether CANA could mitigate HG-induced detrimental responses HCFs. Dose-response assays revealed that 100 nM significantly reduced proliferation migration Furthermore, attenuated mitochondrial reactive oxygen species (ROS) production, a key driver myofibroblast differentiation, suppressed expression SMAD2, activator fibroblasts. Additionally, disrupted calcium (Ca2+) homeostasis, which was ameliorated by treatment. These findings collectively demonstrate exerts protective HCFs improving function, restoring Ca2+ handling, reducing proliferation, migration, activation conditions.

Язык: Английский

The SGLT2 inhibitor canagliflozin attenuates mitochondrial oxidative stress and alterations of calcium handling induced by high glucose in human cardiac fibroblasts DOI
Fahimeh Varzideh, Urna Kansakar, Scott Wilson

и другие.

Cell Cycle, Год журнала: 2025, Номер unknown, С. 1 - 8

Опубликована: Апрель 21, 2025

Cardiac fibrosis and remodeling are critical contributors to heart failure, particularly in the context of diabetes, where hyperglycemia (HG) exacerbates pathological fibroblast activity. Despite known cardiovascular benefits canagliflozin (CANA), its specific effects on human cardiac fibroblasts (HCFs) under HG conditions remain unexplored. We investigated whether CANA could mitigate HG-induced detrimental responses HCFs. Dose-response assays revealed that 100 nM significantly reduced proliferation migration Furthermore, attenuated mitochondrial reactive oxygen species (ROS) production, a key driver myofibroblast differentiation, suppressed expression SMAD2, activator fibroblasts. Additionally, disrupted calcium (Ca2+) homeostasis, which was ameliorated by treatment. These findings collectively demonstrate exerts protective HCFs improving function, restoring Ca2+ handling, reducing proliferation, migration, activation conditions.

Язык: Английский

Процитировано

0