ArticleCellular & molecular biology letters2025
CDK5 regulates PPARγ/NF-κB signaling to exacerbate obesity-related osteoarthritis via modulating macrophage polarization and chondrocyte apoptosis.
Article in Cellular & molecular biology letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Peroxisome proliferator-activated receptor gamma (PPARγ) as a mechano-metabolic transducer: coordinating lipid homeostasis through mechanical cues.Molecular biomedicine · 2026Review
- Artesunate overcomes oxaliplatin resistance in colorectal cancer by inducing ferroptosis through inhibition of the CDK5/Nrf2/GPX4 pathway.Apoptosis : an international journal on programmed cell death · 2026Article
- The context-dependent roles of PPAR-γ in adipocyte differentiation and obesity: a master regulator with dual functions.Frontiers in nutrition · 2026Review
- NF-κB signaling in osteoarthritis: integrating mechanical stress, innate immunity, and cartilage degeneration.Frontiers in immunology · 2026Review
- Targeted regulation of adipose tissue macrophages from an immunometabolic perspective: a novel therapeutic approach for obesity-related metabolic disorders.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundObesity is an important risk factor for osteoarthritis (OA), but the mechanisms associated with OA progression are still not fully understood. The aim of this study was to investigate the role of cyclin-dependent kinase 5 (CDK5) in regulating the peroxisome proliferator-activated receptor gamma (PPARγ)/nuclear factor-κB (NF-κB) signaling pathway and its effect on obesity-related OA.
methodsBy analyzing tissue samples from obese and nonobese patients with OA in conjunction with a high-fat diet (HFD)-induced obese mouse model of OA, we investigated the expression level of CDK5 and its effects on inflammation and apoptosis. The role of CDK5 in macrophage polarization and chondrocyte apoptosis was further explored by gene knockdown and pharmacological intervention.
resultsCDK5 levels were found to be significantly elevated in obese patients with OA, promoting M1 macrophage infiltration and chondrocyte apoptosis. In the model, CDK5 knockdown attenuated cartilage damage and inhibited PPARγ phosphorylation and NF-κB signaling. In vitro experiments showed that overexpression of CDK5 facilitated M1 macrophage polarization and chondrocyte apoptosis, and PPARγ agonists reversed these effects. Mechanically, CDK5 binds to PPARγ to regulate the NF-κB signaling pathway.
conclusionCDK5 promotes the progression of obesity-associated OA through the PPARγ/NF-κB pathway and is a potential therapeutic target in OA, especially in obese patients.
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