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Autophagy is an evolutionarily conserved cellular process that is prominent during bacterial infections. In this review article, we discuss how direct pathogen clearance via xenophagy and regulation of inflammatory products represent dual functions of autophagy that coordinate an effective antimicrobial response. We detail the molecular mechanisms of xenophagy, including signals that indicate the presence of an intracellular pathogen and autophagy receptor-mediated cargo targeting, while highlighting pathogen counterstrategies, such as bacterial effector proteins that inhibit autophagy initiation or exploit autophagic membranes for replication. Pathways that are related to autophagy, including LC3-associated phagocytosis (LAP) and conjugation of ATG8 to single membranes (CASM), are expanding the role of autophagy in antimicrobial defense beyond traditional double-membrane autophagosomes. Examination of Crohn disease-associated genes links impaired autophagy to inflammation and defective bacterial handling. We propose emerging concepts, such as effector-triggered immunity, where autophagy inhibition by pathogens triggers inflammatory defenses and discusses the therapeutic potential of modulating autophagy in infectious and inflammatory diseases.
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http://dx.doi.org/10.1080/27694127.2025.2542904 | DOI Listing |
Surv Ophthalmol
September 2025
Department of Ophthalmology, Affiliated Hospital of Shandong Second Medical University, School of Clinical Medicine, Weifang 261041, China.
Lipid metabolism plays a critical role in maintaining normal physiological functions and is strongly linked to the pathogenesis of ocular vascular diseases. This review examines how disorders of lipid metabolism drive progression in ocular vascular diseases, including diabetic retinopathy, age-related macular degeneration, retinal vascular occlusive diseases, and retinopathy of prematurity. These disorders are classified as a related group due to their common feature of impaired ocular vascularization.
View Article and Find Full Text PDFBiochim Biophys Acta Mol Cell Res
September 2025
Department of Physiology and Pathophysiology, University of Manitoba, Health Sciences Centre, Winnipeg, Canada. Electronic address:
Ferroptosis is a recently discovered lytic form of cell death that is triggered by iron-driven excessive lipid peroxidation and depletion of glutathione and glutathione peroxidase-4 (GPX4). This form of cell death has been linked to a wide range of conditions from cancer to neurodegenerative diseases. Using murine hippocampal HT22 neurons, we aimed to investigate the underlying mechanisms of glutamate-mediated ferroptosis.
View Article and Find Full Text PDFMicrobes Infect
September 2025
Department of Pulmonary and Critical Care Medicine, The Second Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530007, P.R. China. Electronic address:
Background: While autophagy is pivotal in antimicrobial defense, its regulatory role in Talaromyces marneffei (TM) infected bronchial epithelium remains elusive.
Objective: To elucidate the impact of TM infection on autophagy in bronchial epithelial cells and to identify the key molecular regulators involved in this process.
Methods: Primary computational screening identified core autophagy modulators.
Free Radic Biol Med
September 2025
Department of General Surgery, Jiangnan University Medical Center, Wuxi, PR China. Electronic address:
In oxaliplatin-resistant gastric cancer (GC), multi-omics profiling combined with organoid libraries reveals altered metabolic pathways associated with chemoresistance. We identify a novel lactylation modification at K115 of Poly(RC)-binding protein 2 (PCBP2K115la), which confers functional oxaliplatin resistance. Mechanistic studies demonstrate that the long non-coding RNA BASP1-AS1 assembles a complex containing Unc-51 Like Autophagy Activating Kinase 1 (ULK1) and lactate dehydrogenase A (LDHA), thereby activating LDHA enzymatic activity to increase lactate production.
View Article and Find Full Text PDFNeuropharmacology
September 2025
College of Pharmacy, Shanghai University of Medicine and Health Sciences, Shanghai, China. Electronic address:
Aim Of The Study: This study aimed to investigate the protective effects of Geniposide (GEN) against cerebral ischemia-reperfusion injury by targeting the cGAS-STING pathway and modulating autophagy in neuronal cells.
Materials And Methods: In vivo middle cerebral artery occlusion/reperfusion (MCAO/R) model and an in vitro oxygen-glucose deprivation/reperfusion (OGD/R) model to mimic the pathology of cerebral ischemic stroke in humans. Behavioral tests, tissue staining to assess neurological deficits and tissue damage in mice.