ArticleArthritis research & therapy2026
PARP-1 prevents osteoarthritis pathogenesis by inhibiting apoptosis in chondrocytes: an animal study.
Article in Arthritis research & therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Curcumin inhibits chondrocyte apoptosis and inflammation in osteoarthritis via the miR-338-3p/EIF4A1 signaling axis.Hereditas · 2026Article
- Nanotherapeutic Strategies for Osteoarthritis: Targeting Aging, Metabolism and Inflammation.International journal of nanomedicine · 2026Review
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7 authors.
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Abstract
backgroundOsteoarthritis (OA) is a degenerative joint disorder characterized by cartilage breakdown, synovial inflammation, and subchondral bone changes. Chondrocyte apoptosis is a key contributor to cartilage degradation in OA. Poly(ADP-ribose) polymerase-1 (PARP-1), an enzyme involved in DNA repair and apoptosis regulation, is associated with various degenerative diseases. However, its role in OA pathogenesis remains unclear. Therefore, we aimed to investigate the role of PARP-1 in OA pathogenesis using PARP-1 knockout (KO) mice and primary chondrocytes.
methodsOA was induced in wild-type (WT) and PARP-1 KO mice via destabilization of the medial meniscus (DMM). Histological analysis was performed to assess cartilage degeneration, while chondrocyte apoptosis in joint tissues was evaluated using the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. In vitro experiments were conducted using primary chondrocytes isolated from WT and PARP-1 KO mice, and PARP-1 activity was pharmacologically inhibited using 3-aminobenzamide (3-AB). Apoptosis was assessed by TUNEL staining and immunoblot analysis of cleaved PARP-1, poly(ADP-ribose), and caspase-3. The expression of anabolic and catabolic markers was also evaluated under inflammatory conditions.
resultsPARP-1 KO mice exhibited significantly greater cartilage degeneration and chondrocyte apoptosis than did WT controls following DMM surgery. In vitro, PARP-1 deficiency or pharmacological inhibition significantly increased apoptosis and disrupted the balance between anabolic and catabolic factors under inflammatory conditions, thereby exacerbating cartilage degradation.
conclusionsThis study demonstrates that PARP-1 plays a protective role in preserving cartilage integrity under OA conditions. Its deficiency leads to increased apoptosis and cartilage degeneration both in vivo and in vitro. These findings highlight the regulatory role of PARP-1 in OA pathogenesis and underscore the need for further investigation into its underlying mechanisms.
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