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The involvement of ER stress-associated MAPK/JNK signaling in esculetin-induced apoptosis and functional impairment in INS-1 pancreatic β-cells is suggested, providing mechanistic insight into stress-associated β-cell dysfunction.
The results indicate that the PERK pathway is an important contributor to the survival of MOLT-3 cells under basal ER stress, while PERK depletion compromises the resistance of cells to UPR-mediated apoptosis.
In human β cells, pharmacological inhibition of both JNK and p53 improved β cell survival during GRP78 knockdown–induced UPR, and possible therapeutic targets to preserve insulin secretory capacity in diabetes are outlined.
A critical molecular cascade involving suppression of autophagy, induction of ER stress, calcium dysregulation, mitochondrial dysfunction, mitochondrial dysfunction, and oxidative stress that drives GBM cell death is uncovered.
A functional asprosin system is identified in mouse HT-22 hippocampal neurons for the first time, and its direct role in hippocampal neurons remains unclear.
Genistein (GEN) exhibits concentration- and cell-type-dependent biological activities; however, the mechanisms underlying its cytotoxicity remain incompletely understood. This study investigated whether oxidative stress-mediated mitochondrial dysfunction contributes to GEN-induced apoptosis in TM4 mouse Sertoli cells a...
Empagliflozin enhances β-cell proliferation and attenuates ER stress–induced apoptosis in vitro, primarily via downregulation of the PERK–eIF-2α–CHOP pathway.
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