The DOI matches its Crossref record; 46 of the 46 references it cites were found in a registry or an index.
The Impact of Autophagy on Cell Death Modalities
Open accessAbstract
Autophagy represents a homeostatic cellular mechanism for the turnover of organelles and proteins, through a lysosome-dependent degradation pathway. During starvation, autophagy facilitates cell survival through the recycling of metabolic precursors. Additionally, autophagy can modulate other vital processes such as programmed cell death (e.g., apoptosis), inflammation, and adaptive immune mechanisms and thereby influence disease pathogenesis. Selective pathways can target distinct cargoes (e.g., mitochondria and proteins) for autophagic degradation. At present, the causal relationship between autophagy and various forms of regulated or nonregulated cell death remains unclear. Autophagy can occur in association with necrosis-like cell death triggered by caspase inhibition. Autophagy and apoptosis have been shown to be coincident or antagonistic, depending on experimental context, and share cross-talk between signal transduction elements. Autophagy may modulate the outcome of other regulated forms of cell death such as necroptosis. Recent advances suggest that autophagy can dampen inflammatory responses, including inflammasome-dependent caspase-1 activation and maturation of proinflammatory cytokines. Autophagy may also act as regulator of caspase-1 dependent cell death (pyroptosis). Strategies aimed at modulating autophagy may lead to therapeutic interventions for diseases in which apoptosis or other forms of regulated cell death may play a cardinal role.
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Citations
Cites
1 retracted
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Cited by
The Pathogenesis of Sepsis and Potential Therapeutic Targets
Huang, M., Cai, S., & Su, J. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20215376 · Cited by 776
Kalogeris, T., Baines, C. P., Krenz, M., & Korthuis, R. J. (2016) · Comprehensive Physiology · doi:10.1002/cphy.c160006 · Cited by 718
Development of autophagy inducers in clinical medicine
Levine, B., Packer, M., & Codogno, P. (2015) · Journal of Clinical Investigation · doi:10.1172/jci73938 · Cited by 347
A neurogenic perspective of Sarcopenia: time course study of sciatic nerves from aging mice
Krishnan, V. S., White, Z., McMahon, C. D., Hodgetts, S. I., Fitzgerald, M., Shavlakadze, T., Harvey, A. R., & Grounds, M. D. (2016) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlw019 · Cited by 32
Defects in MAP1S-mediated autophagy turnover of fibronectin cause renal fibrosis
Xu, G., Yue, F., Huang, H., He, Y., Li, X., Zhao, H., Su, Z., Jiang, X., Li, W., Zou, J., et al. (2016) · Aging · doi:10.18632/aging.100957 · Cited by 30
Metadata
- Authors
- Ryter, S. W., Mizumura, K., & Choi, A. M. K.
- Venue
- International Journal of Cell Biology
- Publisher
- Wiley
- Published
- 2014
- Volume
- 2014
- Pages
- 1-12
- ISSN
- 1687-8876 (ISSN-L)
- 1687-8884
- OpenAlex
- W2066209509
- Cited by
- 247
- References
- 46
- FWCI
- 22.47
- Type
- journal article
- Language
- en
- Open access
- gold
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
