ArticleInternational journal of molecular medicine2025
PINK1 overexpression suppresses p38 MAPK/NF‑κB signaling to attenuate chondrocyte senescence in osteoarthritis.
Article in International journal of molecular medicine, 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.
- Guanxinshu attenuates atherosclerosis by suppressing Galectin-3-mediated NLRP3 inflammasome activation.Journal of molecular histology · 2026Article
- Mitochondrial Quality Control in Age-Related Diseases: From Molecular Architecture to Precision Therapeutics.Antioxidants (Basel, Switzerland) · 2026Review
- Review
- Dasatinib and quercetin mitigate radiation-induced lung injury by eliminating senescent cells in a rat model.Frontiers in pharmacology · 2026Article
- NF-κB signaling in osteoarthritis: integrating mechanical stress, innate immunity, and cartilage degeneration.Frontiers in immunology · 2026Review
- Traditional Chinese medicine-derived monomers delay osteoarthritis progression by regulating mitochondrial homeostasis.Frontiers in cell and developmental biology · 2026Review
- Energy crisis and cartilage collapse: metabolic reprogramming of chondrocytes in osteoarthritis.Frontiers in immunology · 2026Review
- Mitochondrial quality control modulating chondrocyte behavior and fate in knee osteoarthritis: mechanistic insights and therapeutic prospects.Frontiers in immunology · 2026Review
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Authors and funding
9 authors.
Funding
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Abstract
PTEN‑induced putative kinase 1 (PINK1), a master regulator of mitophagy, is implicated in mitochondrial homeostasis, yet its role in knee osteoarthritis (OA) pathogenesis remains unclear. The present study investigated the mechanisms by which PINK1 modulates chondrocyte senescence during OA progression. Utilizing a destabilization of the medial meniscus‑induced OA murine model, decreased PINK1 expression, impaired mitochondrial function and suppressed mitophagy were observed in OA cartilage.
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