Fisetin ameliorates vascular smooth muscle cell calcification via DUSP1-dependent p38 MAPK inhibition DOI Creative Commons
Mehdi Razazian,

Sheyda Bahiraii,

Azmat Sohail

и другие.

Aging, Год журнала: 2025, Номер unknown

Опубликована: Апрель 2, 2025

Medial vascular calcification is highly prevalent in advanced age and chronic kidney disease (CKD), where it associated with increased risk for cardiovascular events mortality. Vascular smooth muscle cells (VSMCs) actively regulate this process, which can be augmented by inflammation cellular senescence. Thus, the present study investigated impact of fisetin, a flavonol anti-inflammatory senolytic properties, on VSMC calcification. Fisetin treatment suppressed calcific marker expression VSMCs as well p38 MAPK phosphorylation induced pro-calcific conditions. These effects were abolished silencing dual-specificity phosphatase 1 (DUSP1), negative regulator activity. Moreover, knockdown DUSP1 alone was sufficient to increase VSMCs, blunted pharmacological inhibition. Accordingly, aggravated during In addition, fisetin ameliorated uremic conditions exposed serum from dialysis patients. also inhibited ex vivo mouse aortic explants high phosphate cholecalciferol overload model. conclusion, acts potent anti-calcific agent calcification, an effect involving DUSP1-mediated regulation MAPK-dependent signaling.

Язык: Английский

Fisetin ameliorates vascular smooth muscle cell calcification via DUSP1-dependent p38 MAPK inhibition DOI Creative Commons
Mehdi Razazian,

Sheyda Bahiraii,

Azmat Sohail

и другие.

Aging, Год журнала: 2025, Номер unknown

Опубликована: Апрель 2, 2025

Medial vascular calcification is highly prevalent in advanced age and chronic kidney disease (CKD), where it associated with increased risk for cardiovascular events mortality. Vascular smooth muscle cells (VSMCs) actively regulate this process, which can be augmented by inflammation cellular senescence. Thus, the present study investigated impact of fisetin, a flavonol anti-inflammatory senolytic properties, on VSMC calcification. Fisetin treatment suppressed calcific marker expression VSMCs as well p38 MAPK phosphorylation induced pro-calcific conditions. These effects were abolished silencing dual-specificity phosphatase 1 (DUSP1), negative regulator activity. Moreover, knockdown DUSP1 alone was sufficient to increase VSMCs, blunted pharmacological inhibition. Accordingly, aggravated during In addition, fisetin ameliorated uremic conditions exposed serum from dialysis patients. also inhibited ex vivo mouse aortic explants high phosphate cholecalciferol overload model. conclusion, acts potent anti-calcific agent calcification, an effect involving DUSP1-mediated regulation MAPK-dependent signaling.

Язык: Английский

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