ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
The FGF13-Caveolin-1 Axis: A Key Player in the Pathogenesis of Doxorubicin- and D-Galactose-Induced Premature Cardiac Aging.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Aging Disrupts L-type CaCirculation research · 2026Article
- FGF13 alleviates astrocytic apoptosis via JIP2 inhibition in the hippocampus and mitigates depression-like behavior.Journal of neuroinflammation · 2026Article
- FGF 13 functions as a regulator of the ERK/aerobic glycolysis axis in the inflammatory state during septic lung injury.Nature communications · 2026Article
- The mechanisms and therapeutic advances of interactions between breast cancer and cardiovascular diseases.Frontiers in pharmacology · 2026Review
- Multi-Target Botanical Complex Attenuates Cellular Senescence via Bidirectional P21/P53/SIRT1 Regulation: Dual Model Validation.International journal of molecular sciences · 2025Article
- FGF13 prevents age-related hearing loss by protecting spiral ganglion neurons and ribbon synapses from injury.Cell death discovery · 2025Article
- The FGF13-Caveolin-1 Axis: A Key Player in the Pathogenesis of Doxorubicin- and D-Galactose-Induced Premature Cardiac Aging.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Aging reduces the number and function of L-type calcium channels in the membrane of cardiac pacemaker cells.bioRxiv : the preprint server for biology · 2025Article
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Authors and funding
16 authors.
Funding
Abstract
Delaying senescence of cardiomyocytes has garnered widespread attention as a potential target for preventing cardiovascular diseases (CVDs). FGF13 (Fibroblast growth factor 13) has been implicated in various pathophysiological processes. However, its role in premature myocardial aging and cardiomyocyte senescence remains unknown. Adeno-associated virus 9 (AAV9) vectors expressing FGF13 and cardiac-specific Fgf13 knockout (Fgf13KO) mice are utilized to reveal that FGF13 overexpression and deficiency exacerbated and alleviated Doxorubicin/D-galactose-induced myocardial aging characteristics and functional impairment, respectively. Transcriptomics are employed to identify an association between FGF13 and Caveolin-1 (Cav1). Mechanistic studies indicated that FGF13 regulated the Cav1 promoter activity and expression through the p38/MAPK pathway and nuclear translocation of p65, as well as the binding level of PTRF to Cav1 to mediate cardiomyocyte senescence. Furthermore, Cav1 overexpression in murine hearts reversed the alleviatory effects of FGF13 deficiency on the Doxorubicin/D-galactose-induced myocardial aging phenotype and dysfunction. This study has demonstrated that FGF13 regulated the Cav1-p53-p21 axis to augment cardiomyocyte senescence and thereby exacerbated cardiac premature aging and suggests that FGF13 knockdown may be a promising approach to combat CVDs in response to aging and chemotoxicity.
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Registered trials
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