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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]
These metabolic shifts may contribute to improved endurance capacity and delayed fatigue onset during prolonged physical activity
Akter et al
Tzoulaki I, Murray GD, Price JF, Smith FB, Lee AJ, Rumley A, et al
Notably, the deletion of Slc7a11 (which encodes xCT) in animals results in viable offspring 15 , which suggests that tissues (and potentially tumours) can obtain cysteine from another origin
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