Cited by 48Mitochondrial Function and PathologyAutophagy in Disease and TherapyATP Synthase and ATPases Research

The DOI matches its Crossref record; 245 of the 246 references it cites were found in a registry or an index.

Mitochondrial Dynamics in Aging and Disease

Bereiter-Hahn, Jürgen·2014·Progress in molecular biology and translational science

Abstract

Mitochondria are self-replicating organelles but nevertheless strongly depend on supply coded in nuclear genes. They serve many physiological demands in living cells. Supply of the cytoplasm with ATP and engagement in Ca(2+) regulation belong to the main functions of mitochondria. In large eukaryotic cells, in particular in neurons, with their long dendrites and axons, mitochondria have to move to the sites of their action. This trafficking involves several motor molecules and mechanisms to sense the sites of requirements of mitochondria. With aging and as a consequence of some diseases, mitochondrial components may be rendered dysfunctional, and mtDNA mutations arise during the course of replication and by the action of reactive oxygen species. Mutants in motor molecules engaged in trafficking and in the machinery of fusion and fission are causing severe deficiencies on the cellular level; they support neurodegeneration and, thus, cause many diseases. Frequent fusion and fission events mediate the elimination of impaired parts from mitochondria which finally will be degraded by autophagosomes. Extensive fusion provides a basis for functional complementation. Mobility of proteins and small molecules within the mitochondria is necessary to reach the functional goals of fusion and fission, although cristae and a large fraction of proteins of the respiratory complexes proved to be stable for hours after fusion and perform slow exchange of material.

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Crossref · 10.1016/b978-0-12-394625-6.00004-0

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Research works printed but not linked: 1

  1. Lombe, 2002, Mitochondrial fusion in human cells is efficient, requires the inner membrane potential, and is mediated by mitofusins, Mol Biol Cell, 13, 4343, 10.1091/mbc.E02-06-0330 · DOI

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Metadata

Authors
Bereiter-Hahn, J.
Venue
Progress in molecular biology and translational science
Publisher
Elsevier
Published
2014
Volume
127
Pages
93-131
ISSN
1877-1173 (ISSN-L)
OpenAlex
W2405770350
Cited by
48
References
246
Citations by year
2026: 3 · 2025: 4 · 2024: 5 · 2023: 1 · 2022: 2 · 2021: 2 · 2020: 3 · 2019: 6 · 2018: 3 · 2017: 6 · 2016: 9 · 2015: 4
FWCI
8.04
Type
book chapter
Language
en
Open access
closed
Locations
  • Progress in molecular biology and translational science (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › ATP Synthase and ATPases Research
Keywords
mitochondrial dynamics, mitochondrial fusion, mitochondrial fission, mitochondrial biogenesis, mitochondrial trafficking, motor proteins, mitochondrial DNA mutations, reactive oxygen species, neurodegeneration, aging, autophagy, calcium regulation, ATP production, electron transport chain
MeSH terms
Aging, Animals, Humans, Mitochondrial Proteins, Mitochondrial Diseases, Mitochondrial Membranes, Mitochondrial Size, Mitochondrial Dynamics

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