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informatic analysis suggested robust elevated activation of the cysteine proteases Calpains 1 and/or 2 (Capn1/2) in both human and experimental NASH fibrosis (PMID: 36778394)

Other abnormalities include reduced (less complex) branching of some hippocampal neurons and other evidence of alterations in a components of the glutamate neurotransmitter pathway in the hippocampus (Hornig, 2004)

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Blocking CXCR3 signaling using monoclonal antibodies resulted in worsened disease, which was accompanied by reduced recruitment of T cells, ILCs, and macrophages, and a marked increase in neutrophil infiltration

Knockdown of SMAD3 or SMAD4 led to an increase in DLD-K430 acetylation, which remained unresponsive to TGF1 stimulation, while knockdown of SMAD2 did not affect this process (Fig