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First, although we identified and validated PPAR as a key target through bioinformatics and experimentation, we did not perform knockdown or overexpression studies in cell lines to directly confirm a causal relationship between PPAR activity and inhibition of chondrocyte ferroptosis
2022), Nrf2/HO-1 (Han et al
10.3748/wjg.v25.i30.4074 100
We employed diamide, an established thiol-oxidizing agent that oxidizes GSH to GS-SG [22], to induce GSR-mediated NADPH consumption during reduction of GS-SG back to GSH (Fig 1A)
Physiol Rev 78:133
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