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This experiment shows D-LDH to be the most important candidate in providing oxidative stress tolerance followed by GLYI

Damaged AECs release pro-inflammatory and pro-fibrotic mediators, including interleukin (IL) -1 and tumor necrosis factor (TNF) -, which promote fibroblast recruitment, inflammatory cell activation (e.g., neutrophils, Th17, gdT cells), and myofibroblast differentiation, ultimately leading to ECM accumulation and fibrotic tissue remodeling [20, 29, 33, 34]

mediates many of the systemic effects of RA, including the development of C-reactive protein (CRP) (Yusof & Emery, 2013)

The same results were corroborated in the RSL3 model, confirming the mechanism by which theaflavins inhibit cellular ferroptosis by inhibiting HO-1 (Fig

VEGFR2-mediated angiogenesis promotes the formation of new blood vessels, improving blood supply to tissues throughout the body