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The pathogenetic role of SR-B2 (CD36) in atherosclerosis, meta-inflammation, and IR merits particular emphasis

Studying changes in the less affected tissue (BA9) and the primarily affected brain region (CAU) provided insights into the diseases progression

In terms of molecular mechanisms, ZDHHC3 loss of function resulted in reduced palmitoylation modification of inactive rhodopsin 2 (IRHOM2), which in turn promoted its degradation via the ubiquitin-proteasome pathway and ultimately inhibited the activation of the downstream MAP3K7-JNK signaling pathway (158)