CircPAFAH1B2 induces chondrocytes mitochondrial dysfunction and promotes cartilage degeneration through binding molecular chaperone ClpB

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Introduction This study explores the role of circPAFAH1B2 in osteoarthritis (OA) by investigating its influence on nuclear-mitochondrial communication, a largely unexplored area in OA progression. By uncovering how circPAFAH1B2 regulates mitochondrial function, the study aims to identify novel therapeutic targets for OA prevention and treatment. Objectives This study aimed to identify the regulatory role of circPAFAH1B2 in nuclear-mitochondrial communication within chondrocytes and cartilage homeostasis. Methods circPAFAH1B2 expression was determined via quantitative real-time polymerase chain reaction (qRT-PCR) and in situ hybridization. RNA pulldown experiments, proteomic analyses, and RNA immunoprecipitation were conducted to identify the downstream targets of circPAFAH1B2. Gain- and loss-of-function assays were performed to evaluate the regulatory roles of circPAFAH1B2 and the molecular chaperone caseinolytic peptidase B protein homolog (ClpB) in mitochondrial function and chondrocyte homeostasis in cartilage. Cross-linking immunoprecipitation and sequencing were performed to identify binding sites between circPAFAH1B2 and ClpB. Results circPAFAH1B2 was upregulated in OA and localized to the cytoplasm of chondrocytes. In vivo and in vitro experiments demonstrated that increased levels of circPAFAH1B2 induced mitochondrial dysfunction and promoted cartilage degeneration. Mec

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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