Age-Related Deterioration of Mitochondrial Function in the Intestine.


Journal

Oxidative medicine and cellular longevity
ISSN: 1942-0994
Titre abrégé: Oxid Med Cell Longev
Pays: United States
ID NLM: 101479826

Informations de publication

Date de publication:
2020
Historique:
received: 28 05 2020
accepted: 22 07 2020
entrez: 14 9 2020
pubmed: 15 9 2020
medline: 15 5 2021
Statut: epublish

Résumé

Aging is an important and inevitable biological process in human life, associated with the onset of chronic disease and death. The mechanisms behind aging remain unclear. However, changes in mitochondrial function and structure, including reduced activity of the mitochondrial respiratory chain and increased production of reactive oxygen species-thus oxidative damage-are believed to play a major role. Mitochondria are the main source of cellular energy, producing adenosine triphosphate (ATP) via oxidative phosphorylation. Accumulation of damaged cellular components reduces a body's capacity to preserve tissue homeostasis and affects biological aging and all age-related chronic conditions. This includes the onset and progression of classic degenerative diseases such as cardiovascular disease, kidney failure, neurodegenerative diseases, and cancer. Clinical manifestations of intestinal disorders, such as mucosal barrier dysfunction, intestinal dysmotility, and chronic obstipation, are highly prevalent in the elderly population and have been shown to be associated with an age-dependent decline of mitochondrial function. This review summarizes our current understanding of the role of mitochondrial dysfunction in intestinal aging.

Identifiants

pubmed: 32922652
doi: 10.1155/2020/4898217
pmc: PMC7453234
doi:

Substances chimiques

DNA, Mitochondrial 0
Reactive Oxygen Species 0

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

4898217

Informations de copyright

Copyright © 2020 Anna M. Schneider et al.

Déclaration de conflit d'intérêts

The authors declare that they have no conflicts of interest.

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Auteurs

Anna M Schneider (AM)

Department of Pediatrics, Paracelsus Medical University, Salzburg, Austria.

Mihriban Özsoy (M)

Department of Pediatrics, Paracelsus Medical University, Salzburg, Austria.

Franz A Zimmermann (FA)

Department of Pediatrics, Paracelsus Medical University, Salzburg, Austria.
Research Program for Receptor Biochemistry and Tumor Metabolism, Department of Pediatrics, Paracelsus Medical University, Salzburg, Austria.

René G Feichtinger (RG)

Department of Pediatrics, Paracelsus Medical University, Salzburg, Austria.
Research Program for Receptor Biochemistry and Tumor Metabolism, Department of Pediatrics, Paracelsus Medical University, Salzburg, Austria.

Johannes A Mayr (JA)

Department of Pediatrics, Paracelsus Medical University, Salzburg, Austria.

Barbara Kofler (B)

Department of Pediatrics, Paracelsus Medical University, Salzburg, Austria.
Research Program for Receptor Biochemistry and Tumor Metabolism, Department of Pediatrics, Paracelsus Medical University, Salzburg, Austria.

Wolfgang Sperl (W)

Department of Pediatrics, Paracelsus Medical University, Salzburg, Austria.

Daniel Weghuber (D)

Department of Pediatrics, Paracelsus Medical University, Salzburg, Austria.

Katharina Mörwald (K)

Department of Pediatrics, Paracelsus Medical University, Salzburg, Austria.

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