Overexpression of SAT1 promotes OA progression via ferroptosis in vivo.

(A) Representative H&E staining of knee joint sections from sham, OA model, and treatment groups. Severe cartilage degradation and proteoglycan loss are observed in the OA model group, which is partially rescued by treatment. Scale bar: 200 μm. (B)...

وصف كامل

محفوظ في:

التفاصيل البيبلوغرافية
المؤلف الرئيسي:	Jiexiang Yang (19980594) (author)
مؤلفون آخرون:	Jing Jiang (130103) (author), Jing Wang (6206297) (author), Lin Luo (429475) (author)
منشور في:	2025
الموضوعات:	Biochemistry Cell Biology Molecular Biology Cancer prevalent joint disease potential key gene play important roles novel therapeutic strategy medial meniscus ligament experimental results showed cell death characterized associated geo datasets mediated p53 acetylation inhibits p53 acetylation enhancing p53 acetylation intracellular iron accumulation thereby increasing ferroptosis suppressing trim33 expression oa mouse model related gene sat1 xlink "> ferroptosis axis promotes ferroptosis p53 axis xlink "> sat1 promotes related indicators iron overload induce ferroptosis western blot vivo </ vitro </ regulating trim33 oa progresses oa pathogenesis nonapoptotic form lipid peroxidation downregulating trim33 data indicate close association biological functions atdc5 cells analyzing oa
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Overexpression of SAT1 promotes OA progression via ferroptosis <i>in vivo.</i>

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