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Histopathological findings revealed preservation of neural architecture, with reduced axonal degeneration, diminished neuronal loss, and limited formation of cystic cavities, suggesting an attenuation of secondary injury processes (12)
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The most commonly reported gastrointestinal AEs were nausea and diarrhea
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Advanced glycation end products (AGEs) exposure markedly impairs autophagic flux in renal TECs by activating the SMAD3/TFEB axis to suppress lysosome biogenesis and trigger lysosome depletion, leading to the accumulation of autophagosomes and SQSTM1/p62 ( Atg5 aggravates tubule injury and kidney damage, reflected as defective autophagy sensitized proximal TECs to ferroptosis (79)
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