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were the first to show that oral administration of Lactobacillus engineered to express full-length GLP-1 (137) could induce intestinal epithelial cells to transdifferentiate into insulin-producing cells, restoring up to 33% of normal insulin secretory activity

A minimum of 10 PSM was set as a threshold to be required for the detection of a modification

Murine modeling of HFpEF also presents limitations

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Conclusions and future perspectives Therapeutic strategies targeting the ERS-death axis through precise modulation of UPR core pathways (PERK, IRE1, ATF6) and downstream molecules (CHOP, GRP78, XBP1, etc.) have demonstrated significant antitumor potential in preclinical studies