ArticleAutophagy2022
Chloroquine treatment induces secretion of autophagy-related proteins and inclusion of Atg8-family proteins in distinct extracellular vesicle populations.
Article in Autophagy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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Who cites it
45 citing papers in PubMed, 67 citations in OpenAlex.
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- Targeting mitochondrial-ER homeostasis via autophagy inhibition with celastrol-based nanotherapy for triple-negative breast cancer.Journal of nanobiotechnology · 2026Article
- TMEM175 rescues post-infarct cardiac dysfunction via mTORC1-lysosomal axis modulation.Acta pharmacologica Sinica · 2026Article
- Targeting programmed cell death: a novel therapeutic paradigm for cancer based on mode-of-death classification.Apoptosis : an international journal on programmed cell death · 2026Review
- Lomitapide mesylate and lomitapide target ALDOA to inhibit growth and enhance gemcitabine efficacy in PDAC.iScience · 2026Article
- The P2X4 purinergic receptor controls the autophagy-related release of small extracellular vesicles from mammary cancer cells under hypoxia.Cell communication and signaling : CCS · 2026Article
- Tat-HSPE1 suppresses clear cell renal cell carcinoma growth through lysosome-dependent cell death.Frontiers in pharmacology · 2026Article
- The Quartet of Core Oncogenic Drivers in Neuroendocrine Prostate Cancer: Multi-Omics Dataset Integration to Forge a Translational Link Between Biology and Precision Therapy.International journal of biological sciences · 2026Review
- Targeting the secretory autophagy-extracellular vesicle interface: fate decisions and translational opportunities.Frontiers in pharmacology · 2026Review
- Attack cancer: Through autophagic modulations as suppressor or promoter.World journal of clinical oncology · 2025Review
- Improved detection of lipidated Atg8a by immunoblotting inAutophagy · 2025Article
- Autophagic stress activates distinct compensatory secretory pathways in neurons.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- HOPS-dependent vesicle tethering lock inhibits endolysosomal fusions and autophagosome secretion upon the loss of Syntaxin17.Science advances · 2025Article
- Polystyrene nanoplastics trigger pyroptosis in dopaminergic neurons through TSC2/TFEB-mediated disruption of autophagosome-lysosome fusion in Parkinson's disease.Journal of translational medicine · 2025Article
- Dual Roles of Autophagy in Radiation-Induced Brain Injury: Mechanistic Insights and Therapeutic Implications.CNS neuroscience & therapeutics · 2025Review
- Dihydromyricetin restores lysosomal function in Schwann cells to alleviate bortezomib-induced peripheral neuropathy via ERK/TFEB signaling.Archives of toxicology · 2025Article
- Autophagy- and oxidative stress-related protein deregulation mediated by extracellular vesicles of human MJD/SCA3 iPSC-derived neuroepithelial stem cells and differentiated neural cultures.Cell death & disease · 2025Article
- Article
- Inhibition of MALAT1 facilitates ROS accumulation via the Keap1/HO-1 pathway to enhance photodynamic therapy in secondary hyperparathyroidism.Non-coding RNA research · 2025Article
- Inhibiting NLRP3 enhances cellular autophagy induced by outer membrane vesicles fromMicrobiology spectrum · 2025Article
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 3 countries.
Funding
Abstract
Chloroquine (CQ), a lysosomotropic agent, is commonly used to inhibit lysosomal degradation and macroautophagy/autophagy. Here we investigated the cell-extrinsic effects of CQ on secretion. We showed that lysosomal and autophagy inhibition by CQ altered the secretome, and induced the release of Atg8 orthologs and autophagy receptors. Atg8-family proteins, in particular, were secreted inside small extracellular vesicles (sEVs) in a lipidation-dependent manner. CQ treatment enhanced the release of Atg8-family proteins inside sEVs. Using full-length ATG16L1 and an ATG16L1 mutant that enables Atg8-family protein lipidation on double but not on single membranes, we demonstrated that LC3B is released in two distinct sEV populations: one enriched with SDCBP/Syntenin-1, CD63, and endosomal lipidated LC3B, and another that contains LC3B but is not enriched with SDCBP/Syntenin-1 or CD63, and which our data supports as originating from a double-membrane source. Our findings underscore the context-dependency of sEV heterogeneity and composition, and illustrate the integration of autophagy and sEV composition in response to lysosomal inhibition.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.