These insights highlight ALA’s therapeutic potential by inhibiting lung fibroblast activation via TGF-β1 and autophagy proteins (Parkin/LC3) while counteracting metabolic reprogramming in bleomycin-induced fibrosis by suppressing HK2, PFKFB3, Parkin, and LC3 activation [31]. This evidence concerns the gene TGFB1 and fibrosis.