This review delineates how the canonical UPR sensors transduce metabolic stress into pro-inflammatory signaling cascades and discusses the organ-specific consequences of ERS in the liver, pancreas, adipose tissue, vascular endothelium, and hypothalamus, highlighting how this stress sustains a self-reinforcing cycle of tissue injury and metabolic dysfunction.
B. Wen, Xiaojin Wu, Kaiying Zhang et al.· Pharmacological Research· 0 citations
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