Mitochondria: Dynamic Organelles in Disease, Aging, and Development
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Mitochondria are the primary energy-generating system in most eukaryotic cells. Additionally, they participate in intermediary metabolism, calcium signaling, and apoptosis. Given these well-established functions, it might be expected that mitochondrial dysfunction would give rise to a simple and predictable set of defects in all tissues. However, mitochondrial dysfunction has pleiotropic effects in multicellular organisms. Clearly, much about the basic biology of mitochondria remains to be understood. Here we discuss recent work that suggests that the dynamics (fusion and fission) of these organelles is important in development and disease.
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Normally, mitochondria use electrons from different carbon sources to generate a proton gradient across the inner mitochondrial membrane, and the energy of this gradient is used to generate ATP.
“Normally, mitochondria use electrons from different carbon sources to generate a proton gradient across the inner mitochondrial membrane. The energy of this gradient is used to generate ATP (9, 30).”
From Mitochondrial Dysfunction Contributes to Oncogene-Induced Senescence (2009) · cites this paper as [9]
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- Authors
- Chan, D. C.
- Affiliations
- California Institute of Technology (US)
- Corresponding author
- Chan, David C.
- ORCID
- Chan, David C.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2006-06
- Volume
- 125
- Issue
- 7
- Pages
- 1241-1252
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2023542615
- Cited by
- 1,987
- References
- 15
- Citations by year
- 2026: 41 · 2025: 60 · 2024: 83 · 2023: 95 · 2022: 104 · 2021: 116 · 2020: 110 · 2019: 128 · 2018: 115 · 2017: 105 · 2016: 125 · 2015: 95 · 2014: 99 · 2013: 103 · 2012: 127
- FWCI
- 7.53
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 2603 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- CaltechAUTHORS (California Institute of Technology) (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- mitochondria, mitochondrial dynamics, mitochondrial fusion, mitochondrial fission, mitochondrial dysfunction, aging, development (biology), disease, energy metabolism, calcium signaling, apoptosis
- MeSH terms
- Aging, Animals, Disease, DNA, Mitochondrial, Growth, Humans, Membrane Fusion, Metabolic Diseases, Mitochondria, Models, Biological, Mutation, Nerve Degeneration, Nerve Endings, Mitochondrial Diseases
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