Autophagy in Disease and Therapy

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.

The paper shows that amphisomes formed at presynaptic boutons during sustained synaptic activity facilitate protein degradation and local replenishment through mRNA translation.

This study shows that axonal amphisome trafficking in locus coeruleus neurons is regulated by norepinephrine signaling and neuronal activity, with implications for proteostasis.

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 AIP as a regulator that links mTORC1 activation with catabolic metabolism during neonatal development, ensuring metabolic adaptation and survival.

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 a mechanism in plants where clathrin-coated vesicles are selectively degraded via autophagy during osmotic stress to maintain membrane tension and cell integrity.

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 identifies the mitochondria-lysosome axis as critical for maintaining the function of neonatal lysosome-rich enterocytes and preventing premature differentiation.

This study identifies lysosomal RNases and shows specific RNA types are targeted for degradation via autophagy-dependent mechanisms.

The paper develops a functional autophagy gene set signature to classify autophagy states and links autophagy induction and lysosomal activity to poor prognosis in glioblastoma.

This paper develops a novel chloroquine derivative, Lysostilbene-4, which irreversibly damages lysosomes and suppresses their recovery in pancreatic cancer cells.

This study shows that TECPR2 loss causes mitochondrial dysfunction and mitophagy impairment in HSAN9, which can be mitigated by ISR suppression.

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

This study shows that chemical mimetics of the N-degron pathway, called ATLs, can degrade SARS-CoV-2 via autophagy-lysosome system in cells and animals.

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 processing bodies (PBs) as critical for lysosomal quality control and cell survival during recovery from lysosomal damage, distinguishing their role from the acute damage response.

This study identifies a unique lipid composition in plant autophagic membranes, showing phosphatidylglycerol's functional role in autophagy activity.

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 shows autophagy regulates EIN3 stability, affecting Arabidopsis development and stress responses.

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

This study identifies EDC4 and DCP1 as autophagy receptors for P-body turnover in Marchantia polymorpha, revealing lineage-specific adaptations and potential therapeutic applications.

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 autophagy is essential for maintaining HEV function and expansion during inflammation, ensuring proper PNAd production and lymphocyte homing.