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Evidence indicates that using recombinant adeno-associated virus AAV9 in combination with a TGF-/Smad inhibitor can effectively mitigate silicosis-induced PF through ferroptosis inhibition [111]
626 The absence of ALOX5 expression eliminates HTTQ94-induced ferroptosis under oxidative stress conditions, suggesting that ALOX5 is essential for ferroptosis mediated by mutant huntingtin and could be a promising new target for HD treatment
In contrast to mitochondrial and microsomal GSTs, cytosolic GSTs are present in the cytoplasm and are soluble [44]
