Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (586 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The segregation and degradation of various cytoplasmic constituents via engulfment by multivesicular bodies; vacuoles; or autophagosomes and their digestion by lysosomes. It plays an important role in biological metamorphosis and in the removal of bone by osteoclasts. Defective autophagy is associated with various diseases, including neurodegenerative diseases and cancer.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Autophagocytosis; Autophagy, Cellular; Cellular Autophagy; Lipophagy; Ribophagy; Reticulophagy; ER-Phagy; ER Phagy.
Where it fits in the MeSH classification
- Broader topics
- Cell Physiological Phenomena
- Narrower topics
- Autophagic Cell Death; Chaperone-Mediated Autophagy; Efferocytosis; Macroautophagy; Microautophagy; Mitophagy
Related concepts
- Multivesicular Bodies
- Vacuoles
- Autophagosomes
- Lysosomes
- Biological Metamorphosis
- Osteoclasts
- Neurodegenerative Diseases
Research landscape
PubMed indexes 67,198 records tagged with the MeSH heading “Autophagy” (counts retrieved 2026-10-29). 35,283 of them (52.5%) were published from 2020 onward, and the busiest period so far is 2020 onward with 35,283 records.
Reviews account for 11,666 records (17.4%) and meta-analyses for 31. Randomized controlled trials number 68 (0.1%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 0 |
| 2000-2009 | 3,350 |
| 2010-2019 | 28,980 |
| 2020 onward | 35,283 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 11,666 | 17.4% |
| Meta-analyses | 31 | 0.0% |
| Randomized controlled trials | 68 | 0.1% |
Method: PubMed query "Autophagy"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in molecular biology
Molecular biology establishes mechanisms through controlled experiments, often in simplified systems such as purified proteins, cultured cells or model organisms. Such work can show what is possible in a defined system, but whether a pathway matters in a whole organism or in human disease needs further evidence. Check the experimental system, whether findings were reproduced by independent groups, and whether the authors tested the mechanism directly or inferred it from correlation.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Urolithin A activates mitophagy via the AMPK-mTOR axis and modulates the gut-ceramide axis to ameliorate cardiac remodeling in HFpEF | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42432192 · DOI · PMC13434734 |
| Sensing centrosome amplification: the interface between centriole duplication and autophagy | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42324259 · DOI · PMC13439419 |
| VPS33A and VPS18 orchestrate porcine epidemic diarrhea virus replication by modulating autophagic flux | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42537404 · DOI · PMC13432860 |
Urolithin A activates mitophagy via the AMPK-mTOR axis and modulates the gut-ceramide axis to ameliorate cardiac remodeling in HFpEF [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Heart failure with preserved ejection fraction (HFpEF) accounts for nearly half of all heart failure cases.
- Closing excerpt
- Taken together, these findings indicate that UA improves cardiac remodeling in HFpEF by activating mitophagy-dependent mitochondrial quality control and modulating the gut microbiome-ceramide axis, highlighting its potential as a mechanism-based, mitochondria-targeted therapeutic strategy for HFpEF.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (224 words)
Heart failure with preserved ejection fraction (HFpEF) accounts for nearly half of all heart failure cases. However, effective therapies targeting its underlying pathophysiological mechanisms remain lacking. Previous studies have indicated mitochondrial dysfunction and impaired mitophagy as key contributors to HFpEF pathophysiology. In this study, we investigated whether urolithin A (UA), a gut microbiome-derived mitophagy-activating compound, can ameliorate HFpEF. A two-hit mouse model was established using a high-fat diet and Nω-nitro-L-arginine methyl ester, and UA was administered during disease progression. In vitro and in vivo experiments, together with multi-omics analyses, showed that UA alleviated diastolic dysfunction, cardiac hypertrophy, and fibrosis in HFpEF mice. These effects were accompanied by restoration of mitochondrial ultrastructure and enhanced mitochondrial respiration and glycolytic capacity. Notably, UA activated AMPK signaling while inhibiting mTOR, promoting ULK1-dependent autophagy initiation and restoring impaired mitophagic flux. These effects were associated with improved mitochondrial quality control and function. Concurrently, multi-omics analyses revealed that UA remodels the gut microbiome-ceramide axis and reduces circulating ceramide accumulation, thereby alleviating lipotoxic stress. Furthermore, single-nucleus transcriptomic analysis revealed that UA treatment leads to the attenuation of fibrosis-related cellular programming in human induced pluripotent stem cell-derived cardiomyocytes. Taken together, these findings indicate that UA improves cardiac remodeling in HFpEF by activating mitophagy-dependent mitochondrial quality control and modulating the gut microbiome-ceramide axis, highlighting its potential as a mechanism-based, mitochondria-targeted therapeutic strategy for HFpEF.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42432192 · DOI · PMC13434734
Sensing centrosome amplification: the interface between centriole duplication and autophagy [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Multipolar mitotic spindles with extra centrosomes, first observed in cancer cells in the late nineteenth century, remain poorly understood.
- Closing excerpt
- Together our findings add extra dimensions to the roles of RAC1 in cytoskeletal regulation and ARHGAP15 as a potential tumor suppressor.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (149 words)
Multipolar mitotic spindles with extra centrosomes, first observed in cancer cells in the late nineteenth century, remain poorly understood. Here, to address how cells overcome proliferation arrest imposed by centrosome amplification, we describe a genome-wide screen revealing that downregulation of the Wnt, Hippo, Tpr53, PIDDosome, ciliary biogenesis, or autophagy pathways enables proliferation of mouse embryonic stem cells having PLK4-mediated centrosome amplification. We select the tumor suppressor, Guanine-nucleotide Activating Protein ARHGAP15, for further study as its depletion activates autophagy, overcomes centrosome amplification, and enables embryonic fibroblast proliferation. Reduction of centrosomes following ARHGAP15 depletion requires autophagy protein, ATG16L1, which associates with ARHGAP15 when the autophagy pathway is inactive. ARHGAP15 is opposed by Guanine-nucleotide Exchange Factor ARHGEF2, which is activated by the centriolar protein CEP170 to generate RAC1-GTP and promote autophagy. Together our findings add extra dimensions to the roles of RAC1 in cytoskeletal regulation and ARHGAP15 as a potential tumor suppressor.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42324259 · DOI · PMC13439419
VPS33A and VPS18 orchestrate porcine epidemic diarrhea virus replication by modulating autophagic flux [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Completion of autophagy through autophagosome-lysosome fusion represents a critical regulatory checkpoint that is frequently manipulated during viral infection, however, how coronaviruses exploit this terminal step remains incompletely understood.
- Closing excerpt
- Collectively, our findings uncover a coronavirus strategy that actively promotes autophagic completion through VPS33A and VPS18, two core subunits of the HOPS complex, to support replication, thereby establishing autolysosome formation as a critical host process exploited by PEDV.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (213 words)
Completion of autophagy through autophagosome-lysosome fusion represents a critical regulatory checkpoint that is frequently manipulated during viral infection, however, how coronaviruses exploit this terminal step remains incompletely understood. Porcine epidemic diarrhea virus (PEDV), a highly pathogenic alphacoronavirus, has been reported to induce autophagy, but whether and how complete autophagic flux contributes to viral replication is unclear. Here, using a genome-wide CRISPR/Cas9 knockout screen in Vero cells, we identify the HOPS complex subunits VPS33A and VPS18 as essential host factors for PEDV infection. Genetic ablation of either VPS33A or VPS18 profoundly suppresses viral progeny production and arrests autophagic flux at the autophagosome stage, demonstrating that PEDV replication is associated with HOPS-mediated autolysosome formation. Domain-mapping analyses further reveal that the structural integrity of VPS33A and the α-solenoid plus RING domains of VPS18 are indispensable for both autophagosome-lysosome fusion and efficient viral replication. Mechanistically, we show that PEDV non-structural proteins nsp3 and nsp4 physically interact with VPS33A and VPS18. While either protein alone initiates autophagosome formation, their coordinated action contributes to drive complete autophagy in a HOPS-dependent manner. Collectively, our findings uncover a coronavirus strategy that actively promotes autophagic completion through VPS33A and VPS18, two core subunits of the HOPS complex, to support replication, thereby establishing autolysosome formation as a critical host process exploited by PEDV.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42537404 · DOI · PMC13432860
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article The clinical value of using chloroquine or hydroxychloroquine as autophagy inhibitors in the treatment of cancers: A systematic review and meta-analysis [4]
- Research article Mitophagy in the pathogenesis and management of disease [5]
- Research article The prognostic value of autophagy-related markers beclin-1 and microtubule-associated protein light chain 3B in cancers: a systematic review and meta-analysis [6]
- Research article Targeted interplay between bacterial pathogens and host autophagy [7]
- Research article Ferritinophagy: molecular mechanisms and its crosstalk with ferroptosis in chronic respiratory diseases [8]
- Research article Targeting efferocytosis for tissue regeneration: From microenvironment reprogramming to clinical translation [9]
References
- Song H, Yun C, Choi Y, Jeong W, Kim Y, Kim J, et al.. Urolithin A activates mitophagy via the AMPK-mTOR axis and modulates the gut-ceramide axis to ameliorate cardiac remodeling in HFpEF. . 2026. PMID 42432192 · DOI · PMC13434734
- Coelho PA, Fatalska A, Geymonat M, Lattao R, Glover DM. Sensing centrosome amplification: the interface between centriole duplication and autophagy. . 2026. PMID 42324259 · DOI · PMC13439419
- Guo L, Li J, Hao Z, Wang K, Shi Y, Gao F, et al.. VPS33A and VPS18 orchestrate porcine epidemic diarrhea virus replication by modulating autophagic flux. . 2026. PMID 42537404 · DOI · PMC13432860
- Xu R, Ji Z, Xu C, Zhu J. The clinical value of using chloroquine or hydroxychloroquine as autophagy inhibitors in the treatment of cancers: A systematic review and meta-analysis. Medicine (Baltimore). 2018. PMID 30431566 · DOI · PMC6257684
- Wang Q, Sun Y, Li TY, Auwerx J. Mitophagy in the pathogenesis and management of disease. Cell Res. 2026. PMID 41486294 · DOI · PMC12765899
- He Y, Zhao X, Subahan NR, Fan L, Gao J, Chen H. The prognostic value of autophagy-related markers beclin-1 and microtubule-associated protein light chain 3B in cancers: a systematic review and meta-analysis. Tumour Biol. 2014. PMID 24838948 · DOI
- Sudhakar P, Jacomin AC, Hautefort I, Samavedam S, Fatemian K, Ari E, et al.. Targeted interplay between bacterial pathogens and host autophagy. Autophagy. 2019. PMID 30909843 · DOI · PMC6693458
- Ning J, Wen L, Qiao L. Ferritinophagy: molecular mechanisms and its crosstalk with ferroptosis in chronic respiratory diseases. Cell Biol Toxicol. 2026. PMID 41629496 · DOI · PMC12894163
- Li Y, Li P, Song J, Zhang X, Xiao H, Wang R, et al.. Targeting efferocytosis for tissue regeneration: From microenvironment reprogramming to clinical translation. Theranostics. 2026. PMID 41608581 · DOI · PMC12846749
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.