ArticleAging2025
Fisetin ameliorates vascular smooth muscle cell calcification via DUSP1-dependent p38 MAPK inhibition.
Article in Aging, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Plant-Derived Senotherapeutics in Cellular Senescence: A Scoping Review of Preclinical Evidence, Mechanistic Pathways, and Metabolomic-Guided Discovery.International journal of molecular sciences · 2026Article
- Vascular Smooth Muscle Cell Plasticity in Atherosclerosis: Mechanisms, Recent Advances, and Therapeutic Implications.Reviews in cardiovascular medicine · 2026Review
- Role of Inositol Hexakisphosphate Kinases in Vascular Smooth Muscle Cell Calcification.International journal of molecular sciences · 2026Article
- Review
- Integrated Multi-Omics Analyses Identify TYMP as a Candidate Protective Immunoregulatory Marker in CD4⁺ T Cells During Sepsis.Journal of inflammation research · 2026Article
- Vascular Niches Are the Primary Hotspots in Cardiac Aging.Circulation research · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Medial vascular calcification is highly prevalent in advanced age and chronic kidney disease (CKD), where it is associated with increased risk for cardiovascular events and mortality. Vascular smooth muscle cells (VSMCs) actively regulate this process, which can be augmented by inflammation and cellular senescence. Thus, the present study investigated the impact of fisetin, a flavonol with anti-inflammatory and senolytic properties, on VSMC calcification. Fisetin treatment suppressed calcific marker expression and calcification of VSMCs as well as p38 MAPK phosphorylation induced by pro-calcific conditions. These effects were abolished by silencing of dual-specificity phosphatase 1 (DUSP1), a negative regulator of p38 MAPK activity. Moreover, knockdown of DUSP1 alone was sufficient to increase calcific marker expression in VSMCs, effects blunted by pharmacological p38 MAPK inhibition. Accordingly, DUSP1 knockdown aggravated calcification of VSMCs during pro-calcific conditions. In addition, fisetin ameliorated the effects of uremic conditions in VSMCs exposed to serum from dialysis patients. Fisetin also inhibited vascular calcification as well as calcific marker expression
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