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In parallel, ILC3s have emerged as a distinct profibrotic subset, rapidly trafficking from the gut to the injured kidney via the CXCR6-CXCL16 axis, where they directly activate fibroblasts and accelerate kidney fibrosis [93], forming a crucial bridge linking the gut-kidney axis to fibrosis
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Acting directly on adipose tissue without affecting insulin sensitivity or IGF-1 production
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In addition, donors need only be tested once for G6PD deficiency because of its genetic inheritance
doi: 10.3389/fnut.2025.1640156 67
