The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Apoptosis: mechanisms and clinical implications
Abstract
The balance between cell survival and death is under tight genetic control. A multiplicity of extracellular signals and intracellular mediators is involved in maintaining this balance. When the cell is exposed to physical, biochemical or biological injury, or deprived of necessary substances, it activates a series of stress‐response genes. With minimal insults, the cell may recover. With greater insults, single cell death, or apoptosis, results; the cell dies and is recycled to its neighbours. If the insult overwhelms a large number of cells then necrosis ensues, with an accompanying inflammatory response. Dysregulation of the controlling mechanisms of this system results in disease. Deficient apoptosis is associated with cancer, auto‐immunity and viral infections. Excessive apoptosis is associated with ischaemic heart disease, stroke, neurodegenerative disease, sepsis and multiple organ dysfunction syndrome. There are myriad therapeutic options unfolding as understanding is gained of apoptosis and its control.
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Cites
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Apoptosis in the Failing Human Heart
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Cited by
Chiu, J.-J., & Chien, S. (2011) · Physiological Reviews · doi:10.1152/physrev.00047.2009 · Cited by 2,280
CURCUMIN: THE INDIAN SOLID GOLD
Aggarwal, B. B., Sundaram, C., Malani, N., & Ichikawa, H. (2007) · ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY · doi:10.1007/978-0-387-46401-5_1 · Cited by 1,647
Oxidative stress: the mitochondria-dependent and mitochondria-independent pathways of apoptosis
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A review on the mechanisms of blood-flow restriction resistance training-induced muscle hypertrophy
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Metadata
- Authors
- Kam, P. C. A., & Ferch, N. I.
- Venue
- Anaesthesia
- Publisher
- Wiley
- Published
- 2000-11
- Volume
- 55
- Issue
- 11
- Pages
- 1081-1093
- ISSN
- 0003-2409 (ISSN-L)
- 1365-2044
- OpenAlex
- W1969023905
- Cited by
- 455
- References
- 6
- FWCI
- 5.41
- Type
- journal article
- Language
- en
- Open access
- closed
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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.
