ArticleThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology2026
Interleukin-1β-induced arthritis involves chondrocyte oxiapoptophagy.
Article in The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Pro-inflammatory cytokine-induced chondrocyte death contributes to various types of arthritis, including osteoarthritis and rheumatoid arthritis. Recent studies have indicated that oxysterols induce oxiapoptophagy, a form of cell death characterized by oxidative stress, apoptosis, and autophagy. This study aimed to determine whether interleukin-1β (IL-1β)-induced articular cartilage degeneration is associated with chondrocyte oxiapoptophagy. Intra-articular injection of IL-1β into the knee joints of experimental animals induced progressive articular cartilage degeneration and promoted the expression of cholesterol-25-hydroxylase (CH25H), 25-hydroxycholesterol 7α-hydroxylase (CYP7B1), caspase-3, cyclooxygenase-2 (COX-2), and beclin-1. Consistently, IL-1β-stimulated cartilage explants showed proteoglycan loss, and chondrocytes exhibited increased expression and activation of matrix metalloproteinases (MMP-1, MMP-3, MMP-13). IL-1β upregulated the expression of CH25H and CYP7B1, thereby increasing 25-HC production in chondrocytes. Sequentially, IL-1β promoted chondrocyte apoptosis by triggering the caspase cascade, while levels of oxidative stress-related molecules, including reactive oxygen species (ROS), inducible nitric oxide synthase, COX-2, nitric oxide, and prostaglandin E
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