Fasting activates optineurin-mediated mitophagy in chondrocytes to protect against osteoarthritis.
Level 5 - mechanism / opinion, no new human data
Preclinical animal model and mechanistic laboratory study
PubMed 39820028 · doi:10.1038/s42003-025-07541-x
What was done
Researchers evaluated optineurin (OPTN) expression in osteoarthritis patients and examined its functional role using an Optn-knockout mouse model. They assessed how OPTN deficiency affects chondrocyte mitophagy, reactive oxygen species generation, and chondrocyte apoptosis. They also tested the effect of a fasting dietary intervention on OPTN-mediated mitophagy and osteoarthritis progression in mice.
What was found
OPTN was downregulated in patients with osteoarthritis. In knockout mice, OPTN deficiency impaired mitophagy, leading to accumulation of damaged mitochondria, elevated reactive oxygen species, and increased chondrocyte apoptosis. Fasting activated OPTN-mediated mitophagy, maintained mitochondrial homeostasis, and prevented osteoarthritis progression in mice. The abstract reports no numerical values or quantitative effect sizes.
Why it matters
This study identifies optineurin-mediated mitophagy as a protective pathway in chondrocytes and demonstrates that fasting activates this pathway in mice. It highlights optineurin as a candidate therapeutic target for mitigating osteoarthritis progression.
Limits
Findings rely on animal models and in vitro mechanisms, which cannot directly predict clinical outcomes in humans. The abstract does not report sample sizes, specific fasting durations, or numerical statistical outcomes. Clinical efficacy and safety of fasting for human osteoarthritis remain unmeasured.
Cited by
- supports Fasting activates cellular autophagy and mitophagy.