The DOI matches its Crossref record; 32 of the 32 references it cites were found in a registry or an index.
Roles of mitochondria in human disease
Abstract
The chapters throughout this volume illustrate the many contributions of mitochondria to the maintenance of normal cell and tissue function, experienced as the health of the individual. Mitochondria are essential for maintaining aspects of physiology as fundamental as cellular energy balance, the modulation of calcium signalling, in defining cellular redox balance, and they house significant biosynthetic pathways. Mitochondrial numbers and volume within cells are regulated and have an impact on their functional roles, while, especially in the CNS (central nervous system), mitochondrial trafficking is critical to ensure the cellular distribution and strategic localization of mitochondria, presumably driven by local energy demand. Maintenance of a healthy mitochondrial population involves a complex system of quality control, involving degrading misfolded proteins, while damaged mitochondria are renewed by fusion or removed by autophagy. It seems evident that mechanisms that impair any of these processes will impair mitochondrial function and cell signalling pathways, leading to disordered cell function which manifests as disease. As gatekeepers of cell life and cell death, mitochondria regulate both apoptotic and necrotic cell death, and so at its most extreme, disturbances involving these pathways may trigger untimely cell death. Conversely, the lack of appropriate cell death can lead to inappropriate tissue growth and development of tumours, which are also characterized by altered mitochondrial metabolism. The centrality of mitochondrial dysfunction to a surprisingly wide range of major human diseases is slowly becoming recognized, bringing with it the prospect of novel therapeutic approaches to treat a multitude of unpleasant and pervasive diseases.
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Cites
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Cited by
Mikkelsen, K., Stojanovska, L., Polenakovic, M., Bosevski, M., & Apostolopoulos, V. (2017) · Maturitas · doi:10.1016/j.maturitas.2017.09.003 · Cited by 1,072
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Raffaello, A., De Stefani, D., Sabbadin, D., Teardo, E., Merli, G., Picard, A., Checchetto, V., Moro, S., Szabò, I., & Rizzuto, R. (2013) · The EMBO Journal · doi:10.1038/emboj.2013.157 · Cited by 490
Mitochondria: A central target for sex differences in pathologies
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Wang, Z., Liu, D., Varin, A., Nicolas, V, Courilleau, D., Mateo, P., Caubere, C., Rouet, P., Gomez, A.-M., Vandecasteele, G., et al. (2016) · Cell Death & Disease · doi:10.1038/cddis.2016.106 · Cited by 106
“sufficient energy for cell functions, maintain mitochondrial membrane integrity and avoid excessive cell death.(4,5) Moreover, mitochondria may participate in Ca homeostasis via matrix Ca accumulation through the mitochondrial Ca uniporter (MCU), Ca release into the cytosol and propagation to other mitochondria, notab…”
Background
Metadata
- Authors
- Duchen, M. R., & Szabadkai, G.
- Venue
- Essays in Biochemistry
- Publisher
- Portland Press Ltd.
- Published
- 2010-06-14
- Volume
- 47
- Pages
- 115-137
- ISSN
- 0071-1365 (ISSN-L)
- 1744-1358
- OpenAlex
- W2057691269
- Cited by
- 168
- References
- 32
- FWCI
- 5.20
- Type
- journal article
- Language
- en
- Open access
- closed
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