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The accumulation of harmful metabolites and depletion of protective metabolites contribute to fibrosis progression through various mediators, including the renin-angiotensin system, reactive oxygen species, Toll-like receptor 4, aryl hydrocarbon receptor, inhibitor of kappa B/nuclear factor kappa B, and Kelch-like ECH-associated protein 1/nuclear factor erythroid 2-related factor 2 pathways

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The triple-receptor mechanism, particularly the added glucagon receptor activation, accelerates results

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The B7:CD28 family and friends: Unraveling coinhibitory interactions