MAP1LC3B (Microtubule Associated Protein 1 Light Chain 3 Beta)

Beclin1 knockdown and DHODH overexpression can reduce DOX-induced liver injury by preventing ferroptosis and autophagy.

The presence of DAO in peroxisomes, autophagosomes, lysosomes, and exosomes indicated diverse intracellular localization within CPECs. This distribution may enable efficient metabolism of blood-derived D-serine in CPECs.

This study suggests that CRO may reduce ferritinophagy-induced colonic oxidative damage in rats via modulating AKT/mTORC1/ULK1. Ferritinophagy as an attractive therapeutic target in different experimental and clinical conditions deserves further investigation.

Collectively, our findings demonstrate that NaF activates the PINK1/Parkin-mediated mitophagy pathway; however, incomplete autophagic degradation leads to mitochondrial dysfunction and neuronal apoptosis, contributing to developmental neurotoxicity. Importantly, melatonin mitigates these adverse effects, suggesting its potential as a therapeutic agent for preventing fluoride-induced neurodevelopmental impairment through modulation of the PINK1/Parkin signaling axis.

Activation of the HIF-1α/BNIP3 pathway drives protective mitophagy to suppress the NLRP3 inflammasome in neuronal cells, thereby conferring neuroprotection against CIRI. This study provides mechanistic insights into the protective role of HIF-1α/BNIP3-mediated mitophagy against CIRI, highlighting its potential as a therapeutic target for ischemic injury.

NAC exerted beneficial effects mainly in the early postpartum period but was insufficient later. Furthermore, NAC induced sex-specific effects in the offspring, with a more substantial impact observed in males.

BC emerges as a promising therapeutic agent for TNBC by targeting SESN2 and MAP1LC3B, modulating associated signaling pathways, and inducing ferroptosis and mitophagy. These findings provide the basis for further investigation of BC's potential as a targeted therapy for TNBC.

The mice were randomly divided into a CIA model group (MO group), melittin acupoint subcutaneous injection group (ST group), melittin acupoint intramuscular injection group (IT group), and methotrexate group (MTX group), with an additional normal control group (NC group) established...WB analysis showed elevated levels of Unc-51-like autophagy activating kinase 1 (ULK1), beclin-1 (P<0.01), and microtubule-associated protein 1 light chain 3 II (LC3II) (P<0.05), and reduced phosphorylation of PI3K, AKT, and mTOR (P<0.05). MAI alleviates RA symptoms by inhibiting the PI3K/AKT/mTOR pathway and promoting autophagy.

By the invasion test, compound 8 was found to restrain the invasion of PANC-1 cells. In autophagy assay, we observed increased microtubule-associated protein 1 light chain 3 (LC3) by immunofluorescence in the compound 8-treated group.

Compared with the control group, the experimental group exhibited elevated expression levels of EMT-associated protein E-cadherin, reduced expression level of vimentin, increased expression levels of autophagy-related protein 5(ATG5) and LC3B, and decreased expression level of sequestosome 1(p62). In conclusion, emodin can promote the autophagy of human nasopharyngeal carcinoma cells and inhibit the proliferation, cloning, EMT, and pelletizing ability of tumor stem cells.

RETREG1 knockout abolishes degradation of ER-retained SERINC5, whereas endolysosomal turnover of surface SERINC5 remains partially intact, demonstrating that glycoGag utilizes dual ER-phagy and endolysosomal routes to suppress SERINC5. These findings expand the functional repertoire of RETREG1 in autophagy, identify that retroviruses repurpose micro-ER-phagy to circumvent SERINC5-mediated restriction, and reveal ER-phagy as an understudied battleground in the ongoing arms race between cellular restriction factors and viral accessory proteins.

Rebamipide acts as a promising preventive agent against cadmium-induced nephrotoxicity, through its potent antioxidant and anti-inflammatory mechanisms.