CASP12 (Caspase 12 (Gene/Pseudogene))

Our histological results showed that BSFL extract (360 mg/kg) could reduce steatosis, cellular swelling, and lobular inflammation induced after AF exposure. The results of this study indicate that BSFL extract, as a valuable bioactive substance with antioxidant properties, may attenuate biochemical indices, oxidative stress, and inflammation caused by AF-induced hepatotoxicity.

HMB protects lungs in experimental sepsis by inhibiting NF-κB inflammation, reducing ER and mitochondrial apoptosis, and boosting antioxidant defenses via NRF2/GPX4. These findings support its potential as adjunct therapy for sepsis-induced ALI.

The USMB group exhibited the lowest mitochondrial membrane potential and the highest Ca2+ fluorescence intensity. These findings indicate that USMB activates ER stress via Piezo1, induces mitochondrial dysfunction, elevates intracellular Ca2+, and thereby promotes apoptosis in breast cancer cells.​​.

MM/GBSA free energy and ligand efficiency calculations further confirmed its favorable binding characteristics. Collectively, these findings demonstrate that Kaempferol induces colorectal cancer cell death through ER stress-mediated apoptosis and BcL-2 modulation, positioning it as a promising candidate for further preclinical development.

Molecular docking of Lorestanol with MRP1 further supported its binding within the substrate site, highlighting interactions with key amino acid residues. These findings suggest that Lorestanol significantly enhances cisplatin efficacy and may help overcome chemotherapy resistance in ovarian cancer.

AMPK and P53 act to inhibit lung adenocarcinoma progression. CPS1 promotes the progression of lung adenocarcinoma by suppressing ammonia-induced activation of the ROS/AMPK/P53/LKB1 signaling pathway.

These findings underscore the promise of GSK2606414 and cisplatin co-treatment as a potent strategy to counteract ovarian cancer resistance. This combination could potentially advance therapeutic outcomes and provide a new pharmacological approach to resistant cancers.

Noteworthy, the co-administration of NE100 reduced the advantageous effects of fluvoxamine, indicating the involvement of sigma-1 receptor in mediating the observed antipsychotic effects. Thus, sigma-1-mediated signaling pathways could be therapeutic targets for preventing or slowing schizophrenia progression.

ATO induces ICD in HCC via a ROS/ERS signaling axis, thereby amplifying antitumor immune responses and synergizing with PD-1 blockade. These findings support the clinical evaluation of ATO-PD-1 inhibitor combinations to improve outcomes in HCC patients.

These results suggest that ERS exists in the OGD/R-injured H9c2 cell model, and TFDM can effectively inhibit ERS-induced apoptosis. The mechanism may be related to the downregulation of ERS pathway-related proteins and apoptotic proteins.

The activation of ER stress and mitochondrial dysfunction pathways following MCAO led to oligodendrocyte damage and apoptosis. AMX0035 can inhibit these pathways, reduce oligodendrocyte apoptosis, and alleviate demyelination, thereby improving PSCI.

The expression of Bax and caspase-12 was found to be upregulated, while the expression of Bcl-2 was reduced. This study is the first to demonstrate that silencing the PERK gene through miR-204-5p significantly inhibits cell growth and promotes ER-stress-induced apoptosis in ovarian cancer cells.