Mitochondria and the Autophagy–Inflammation–Cell Death Axis in Organismal Aging
Open accessAbstract
Alterations of mitochondrial functions are linked to multiple degenerative or acute diseases. As mitochondria age in our cells, they become progressively inefficient and potentially toxic, and acute damage can trigger the permeabilization of mitochondrial membranes to initiate apoptosis or necrosis. Moreover, mitochondria have an important role in pro-inflammatory signaling. Autophagic turnover of cellular constituents, be it general or specific for mitochondria (mitophagy), eliminates dysfunctional or damaged mitochondria, thus counteracting degeneration, dampening inflammation, and preventing unwarranted cell loss. Decreased expression of genes that regulate autophagy or mitophagy can cause degenerative diseases in which deficient quality control results in inflammation and the death of cell populations. Thus, a combination of mitochondrial dysfunction and insufficient autophagy may contribute to multiple aging-associated pathologies.
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Primary lysosomal dysfunction may impair mitophagic responses, negatively affecting the mitochondrial network.
“Moreover, primary lysosomal dysfunction may negatively affect the mitochondrial network as a consequence of impaired mitophagic responses (which normally target damaged or dysfunctional mitochondria to lysosomes for degradation) [779, 780].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [779]
Insufficient mitophagy and autophagy contribute to the accumulation of mutant mtDNA and are a factor in aging and age-related diseases.
“As with the fission and fusion processes, insufficient mitophagy and autophagy contribute to the accumulation of mutant mtDNA and are a factor in aging and age-related diseases (Gaziev et al., 2014; Green et al., 2011; Hubbard et al., 2012; Rubinsztein et al., 2011).”
From Role of the mitochondrial DNA replication machinery in mitochondrial DNA mutagenesis, aging and age-related diseases (2017) · cites this paper as Green et al., 2011
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Autophagy During Cardiac Stress: Joys and Frustrations of Autophagy
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The Effect of Aging on Human Skeletal Muscle Mitochondrial and Intramyocellular Lipid Ultrastructure
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The Parkinson-associated protein PINK1 interacts with Beclin1 and promotes autophagy
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Human IRGM regulates autophagy and cell-autonomous immunity functions through mitochondria
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Nix directly binds to GABARAP: A possible crosstalk between apoptosis and autophagy
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Self-citationMitochondrial autophagy and injury in the liver in α 1 -antitrypsin deficiency
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Coenzyme Q deficiency triggers mitochondria degradation by mitophagy
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Deletion of the Huntingtin Polyglutamine Stretch Enhances Neuronal Autophagy and Longevity in Mice
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Parkin Mono-ubiquitinates Bcl-2 and Regulates Autophagy
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- Authors
- Green, D. R., Galluzzi, L., & Kroemer, G.
- Affiliations
- St. Jude Children's Research Hospital (US)
- Université Paris-Sud (FR)
- Inserm (FR)
- Corresponding author
- Green, Douglas R.
- Kroemer, Guido
- Venue
- Science
- Published
- 2011-08-26
- Volume
- 333
- Issue
- 6046
- Pages
- 1109-1112
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC3405151
- OpenAlex
- W1976391651
- Cited by
- 1,245
- References
- 138
- Citations by year
- 2026: 55 · 2025: 83 · 2024: 86 · 2023: 85 · 2022: 111 · 2021: 100 · 2020: 91 · 2019: 73 · 2018: 71 · 2017: 83 · 2016: 70 · 2015: 89 · 2014: 67 · 2013: 77 · 2012: 90
- FWCI
- 9.23
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of General Medical Sciences (R01GM096208, R37GM052735)
- National Institute of Allergy and Infectious Diseases (R01AI040646, R01AI047891)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- mitochondria, aging, autophagy, mitophagy, inflammation, cell death, mitochondrial dysfunction, apoptosis, necrosis, mitochondrial membrane permeabilization, degenerative diseases
- MeSH terms
- Aging, Animals, Autophagy, Humans, Inflammation, Mitochondria, Necrosis, Cellular Senescence, Cell Death, Apoptosis, Neurodegenerative Diseases
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