Ferroptosis inhibition and mitochondrial rescue: a novel mechanism of emodin in rheumatoid arthritis - PubMed
4 hours ago
- #emodin
- #rheumatoid-arthritis
- #ferroptosis
- Emodin (EMO) shows therapeutic effects in rheumatoid arthritis (RA) by inhibiting ferroptosis and rescuing mitochondrial function.
- RA is characterized by chronic synovitis and joint destruction, with ferroptosis implicated in its pathogenesis.
- Key regulators of ferroptosis, GPX4 and ACSL4, play significant roles in RA, with EMO modulating their expression.
- EMO treatment in mice and macrophages reduced inflammation, oxidative stress, and bone destruction while restoring iron and mitochondrial homeostasis.
- The study highlights ferroptosis as a novel therapeutic target in RA and supports EMO as a potential adjunctive treatment.