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Together with the earlier made observations that PINK and Parkin levels are reduced in hearts of diabetic mice, one can speculate that either mitophagy is impaired in later stages of DM, or that the induction of mitophagy may not be sufficient to balance the mitochondrial damage caused by other mechanisms of DbCM [9192]

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Early research has shown that proinflammatory cytokines (e.g., tumor necrosis factor-α [TNF-α] and interferon-γ) impair TJ integrity ( Regulatory Mechanisms of the TJ Barrier The innate immune system can sense pathogen-associated molecular patterns via pattern recognition receptors, including Toll-like receptors (TLRs) and nucleotide-binding oligomerization domain-containing proteins (i.e., NOD1 and NOD2) ( in vitro ( in vitro and in vivo ( Endogenous machinery to suppress TJs is regulated by zonulin, a eukaryotic analog of the ZO toxin produced by Vibrio cholerae ( ex vivo ( The biological impact of zonulin on the intestinal epithelial barrier and the immune system has been defined in studies of zonulin-overexpressing mice, in which the mouse Hp1 gene is replaced with the human Hp2 (h Hp2 ) gene ( Hp2 knock-in enhanced intestinal permeability and promoted the development of dextran sodium sulfate (DSS)-induced colitis ( Hp2 knock-in mice also exhibited a proinflammatory immune response mediated by RORγt + cells, especially IL7R + CD3 - RORγt + (most likely, group 3) innate lymphoid cells in the small intestine ( Table 1 )