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Figure 12. Schematic illustration of mechanisms involved in the protective effects of fisetin during VSMC calcification. Mineral stress with disturbed phosphate and calcium homeostasis may trigger activation of pro-calcific signaling including phosphorylation and activation of p38 MAPK in VSMCs, which leads to a pro-calcific environment causing vascular calcification. Fisetin, a natural flavonol, induces the dual-specificity phosphatase 1 (DUSP1). Fisetin thereby inactivates p38 MAPK signaling through DUSP1 and inhibits further pro-calcific signaling and calcification of VSMCs.
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Credit: Copyright: © 2025 Razazian et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
“Fisetin treatment suppressed calcific marker expression and calcification of VSMCs as well as p38 MAPK phosphorylation induced by pro-calcific conditions.”
BUFFALO, NY — May 6, 2025 — A new research paper was published in Aging (Aging-US) Volume 17, Issue 4, on April 2, 2025, titled “Fisetin ameliorates vascular smooth muscle cell calcification via DUSP1-dependent p38 MAPK inhibition.”
In this study, researchers at Johannes Kepler University Linz found that fisetin, a natural substance found in fruits and vegetables, helps protect blood vessels from hardening, which is a common problem in older adults and people with kidney disease. This discovery highlights fisetin’s potential to prevent vascular calcification and reduce cardiovascular damage caused by aging and chronic kidney disease.
The research, led by first author Mehdi Razazian and corresponding author Ioana Alesutan, focused on vascular calcification—a condition in which blood vessels stiffen due to calcium deposits. This process is common in aging and chronic kidney disease and increases the risk of heart attacks and strokes. Using human and mouse study models, the researchers tested fisetin’s ability to prevent this calcification in vascular smooth muscle cells (VSMC), which play a key role in maintaining vessel health. Fisetin, known for its anti-inflammatory and antioxidant properties, significantly reduced calcium buildup and calcification markers under stress conditions that mimic disease.
The team also discovered that fisetin suppresses activity in a signaling pathway called p38 MAPK, which is known to promote calcification. This effect depends on a protein called DUSP1. When DUSP1 was blocked, fisetin could no longer protect the cells, showing that this protein is essential for its anti-calcification activity. The researchers confirmed fisetin’s protective effects in isolated mouse arteries and in living mice treated with high doses of vitamin D, which typically increases arterial calcification.
“Mechanistically, fisetin requires the phosphatase DUSP1 to inhibit p38 MAPK in order to mediate its protective effect on VSMC calcification.”
Importantly, the researchers tested fisetin under conditions similar to human disease. When VSMCs were exposed to blood serum from kidney dialysis patients—a condition known to trigger vascular calcification—fisetin again reduced calcium buildup and protected the cells. These findings suggest fisetin could be useful in countering the harmful vascular effects seen in chronic kidney disease.
This study adds to growing evidence that fisetin may protect blood vessels from aging-related damage. While more research is needed before it can be used in clinical treatments, the study highlights fisetin as a promising candidate for slowing or preventing vascular calcification. The findings could have broad implications for aging populations and individuals with kidney disease, who are at greater risk for heart problems due to vascular stiffening.
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Corresponding author: Ioana Alesutan – [email protected]
Keywords: aging, vascular calcification, vascular smooth muscle cells, fisetin, dual-specificity phosphatase 1, p38 MAPK
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Journal
Aging-US
DOI
10.18632/aging.206233
Method of Research
News article
Subject of Research
Cells
Article Title
Fisetin ameliorates vascular smooth muscle cell calcification via DUSP1-dependent p38 MAPK inhibition
Article Publication Date
2-Apr-2025
COI Statement
The authors declare that they have no conflicts of interest.
Media Contact
Ryan Braithwaite
Impact Journals LLC
Journal
Aging-US
DOI
10.18632/aging.206233
Journal
Aging-US
DOI
10.18632/aging.206233
Method of Research
News article
Subject of Research
Cells
Article Title
Fisetin ameliorates vascular smooth muscle cell calcification via DUSP1-dependent p38 MAPK inhibition
Article Publication Date
2-Apr-2025
COI Statement
The authors declare that they have no conflicts of interest.
Keywords
/Life sciences/Cell biology/Cells/Vascular cells
/Life sciences/Cell biology
/Health and medicine
/Scientific community/Academic publishing/Publishing industry/Open access
/Scientific community/Academic publishing/Publishing industry/Digital publishing
/Scientific community/Academic publishing/Publishing industry
/Scientific community/Academic publishing/Peer review
/Scientific community/Academic publishing
/Scientific community/Academic publishing/Academic journals
/Scientific community
/Scientific community/Scientific publishing
bu içeriği en az 2000 kelime olacak şekilde ve alt başlıklar ve madde içermiyecek şekilde ünlü bir science magazine için İngilizce olarak yeniden yaz. Teknik açıklamalar içersin ve viral olacak şekilde İngilizce yaz. Haber dışında başka bir şey içermesin. Haber içerisinde en az 12 paragraf ve her bir paragrafta da en az 50 kelime olsun. Cevapta sadece haber olsun. Ayrıca haberi yazdıktan sonra içerikten yararlanarak aşağıdaki başlıkların bilgisi var ise haberin altında doldur. Eğer yoksa bilgisi ilgili kısmı yazma.:
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Tags: aging and kidney diseasedual-specificity phosphatase 1fisetin health benefitsflavonols and cardiovascular healthmechanisms of arterial hardening preventionmineral stress and calcificationnatural compounds for artery healthnatural remedies for kidney healthp38 MAPK signaling pathwaypreventing vascular calcificationpro-calcific signaling inhibitionvascular smooth muscle cells
