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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]

4547 However, recent investigations have raised questions about the exclusive role of pyroptosis in APAP-induced hepatocyte loss

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

TB-500 and BPC-157 are frequently referenced together in laboratory research settings due to their complementary research pathways