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The disease spectrum varies enormously due to the interaction of AFs-induced oxidative stress, apoptosis, necrosis of proximal tubular epithelium, oxidative DNA damage, p53 disruption, bioactivation, disruption of regeneration fidelity [31, 32, 37], immune dysregulation, enhancement of neutrophil elastase-induced damage [32], epigenetic modification, disruption of protein synthesis, impairment of sound cellular regeneration, disturbed cell cycle in S phase, lipotoxicity, mitochondrial dysfunction, upregulation of micro RNA, autophagy, stimulation of transforming growth factor pathways, augmentation of Escherichia coli toxicity, dysbiosis [38], and others [28, 32, 38]

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It has been found that tryptophan catabolic processes to acetyl-CoA, tryptophan catabolic processes to kynurenine, and tryptophan catabolic process were enriched in the human AAA group[91]

It has been shown that there is activation of the JNK pathway following exposure to various stress factors, including cytokines, growth factors, oxidative stress, and response signals to unfolded proteins or A peptides