Evidence map›Paper›PMID 32922652›Full record

ReviewOxidative medicine and cellular longevity2020

Age-Related Deterioration of Mitochondrial Function in the Intestine.

Anna M Schneider, Mihriban Özsoy, Franz A Zimmermann, René G Feichtinger, Johannes A Mayr, Barbara Kofler, Wolfgang Sperl, Daniel Weghuber, Katharina Mörwald

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Oxidative medicine and cellular longevity · 2021
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Anna M SchneiderDepartment of Pediatrics, Paracelsus Medical University, Salzburg, Austria.
Mihriban ÖzsoyDepartment of Pediatrics, Paracelsus Medical University, Salzburg, Austria.
Franz A ZimmermannDepartment of Pediatrics, Paracelsus Medical University, Salzburg, Austria.ORCID https://orcid.org/0000-0002-5380-6783
René G FeichtingerDepartment of Pediatrics, Paracelsus Medical University, Salzburg, Austria.ORCID https://orcid.org/0000-0002-4215-8258
Johannes A MayrDepartment of Pediatrics, Paracelsus Medical University, Salzburg, Austria.ORCID https://orcid.org/0000-0001-6970-336X
Barbara KoflerDepartment of Pediatrics, Paracelsus Medical University, Salzburg, Austria.ORCID https://orcid.org/0000-0002-1198-4776
Wolfgang SperlDepartment of Pediatrics, Paracelsus Medical University, Salzburg, Austria.
Daniel WeghuberDepartment of Pediatrics, Paracelsus Medical University, Salzburg, Austria.ORCID https://orcid.org/0000-0002-4389-0379
Katharina MörwaldDepartment of Pediatrics, Paracelsus Medical University, Salzburg, Austria.
Paracelsus Medical University · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

AgingAnimalsDNA, MitochondrialHumansIntestinesMitochondriaMutationReactive Oxygen SpeciesDNA, MitochondrialReactive Oxygen Species

Identifiers

PMID32922652
PMCPMC7453234
OpenAlexW3064268913

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.