Autophagy in Disease and Therapy

The paper identifies endosomal microautophagy (eMI) activation in trout hepatocytes under specific stress conditions and suggests its compensatory role when CMA is impaired.

This study identifies ERC1 as a protein that forms biomolecular condensates to recruit ATG8 and NBR1, promoting autophagosome formation and enhancing heat tolerance in Arabidopsis.

This study investigates how chemerin-CMKLR1 signaling differentially affects mitochondrial dysfunction, oxidative stress, and autophagy in microglia and neurons under OGD/R conditions.

This study investigates the role of Cho1-encoded phosphatidylserine synthase in autophagy, showing its essential role in macroautophagy and its interaction with the ubiquitination system in microautophagic lipophagy.

The paper identifies Rab7-Epg5 and Rab39-ema modules that coordinate autophagosome positioning toward the ncMTOC for efficient lysosomal fusion in Drosophila fat cells.

This study shows that autophagy in adipocytes limits obesity-related fibrosis by controlling purine nucleoside metabolism and macrophage polarization.

This study shows TRAF6 regulates glucose homeostasis via mitophagy in islets, with both Parkin-dependent and -independent pathways involved.

This study shows mitochondrial dysfunction causes early endosome aggregation and cargo trafficking defects via ROS-induced microtubule reorganization, highlighting mitochondria's role in endocytic trafficking.

This study shows that HLH-30/TFEB expands neuronal lysosomal capacity in early adulthood, protecting dendrite maintenance during aging in C. elegans.

This study identifies glycophagy dysregulation as a mechanism of diabetic heart disease and shows that Gabarapl1 gene therapy improves cardiac function in diabetic mice and human cardiac organoids.

This study identifies non-canonical autophagy pathways, including LC3-associated phagocytosis and STIL, that mediate host defense against pneumococcal infection in zebrafish.

This paper describes a method to isolate functional lysosomes from mouse skeletal muscle tissue, preserving their structure and function, and demonstrates reduced lysosomal activity in aging muscle.

The paper identifies PS clustering by membrane receptors as a trigger for LC3-associated phagocytosis (LAP), revealing a novel PS-mediated signal transduction mechanism.

This study shows that phase separation of the Atg1 complex forms the PAS, which facilitates Atg8 lipidation and autophagosome formation in yeast.

The paper identifies BLTP3A as a protein associated with late endocytic membranes and shows it interacts with the CASM pathway to respond to lysosome damage.

This study shows Atg11 binds autophagosomal-like membranes via an amphipathic helix, clustering vesicles on cargo mimetics to initiate mitophagy.

This study shows that aging impairs proteostatic mechanisms in mice with cardiac-specific over-expression of adenylyl cyclase VIII, leading to accelerated heart aging and cardiomyopathy.

The paper shows that peri-mitochondrial actin filaments (ADA) inhibit Parkin assembly by disrupting ER-mitochondrial contacts, delaying mitophagy after acute damage and blocking it during chronic dysfunction.

This study identifies ULK1's role in bacterial ubiquitylation and p62 recruitment during xenophagy, showing its importance in autophagic clearance of Listeria monocytogenes.

This study identifies Rab39 as a regulator of autophagy at presynaptic terminals in Drosophila, showing its role in trafficking Atg9 vesicles and its link to neurodegeneration.

The paper shows that different ATG8 isoforms in Arabidopsis have specialized functions in autophagy, as demonstrated by a mutant lacking all nine isoforms and complementation experiments.

This study identifies PEX14 as a molecular link between optineurin and pexophagy, elucidating its role in recruiting autophagic machinery for peroxisome degradation.

The paper uses time-course RNA-seq to study muscle remodeling in Drosophila, identifying BNIP3-mediated mitophagy as critical for mitochondrial degradation during this process.

This study evaluates 104 2022 papers claiming to show autophagic cell death, finding most lack causality evidence and suffer from methodological and terminological issues.

The paper identifies a novel stress response pathway, MitoSR, triggered by mitochondrial damage that enhances mitophagy by degrading negative regulators in neurons.

This study shows that intrinsically disordered regions (IDRs) of ER-phagy receptors drive ER fragmentation, not their membrane-remodeling domains.

The paper shows that restoring GTP levels in aged neurons improves endocytosis and autophagy, reducing Aβ aggregates and oxidative damage.

This study uses CRISPR/Cas9 to knockout Arabidopsis ATG8 genes, revealing their redundant and regulatory roles in autophagy, with Clade I and II ATG8s showing overlapping functions and interactions with RABG3 proteins.

This study shows that elevated O-GlcNAcylation reduces mitophagy in astrocytes and alters glia homeostasis in the dentate gyrus.