Evidence map›Paper›PMID 33864592›Full record

ArticleGeroScience2021

An energetics perspective on geroscience: mitochondrial protonmotive force and aging.

Brandon J Berry, Matt Kaeberlein

Open access · bronzeAbstract read
In one paragraph

Article in GeroScience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.0field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Mitochondria makeover: unlocking the path to healthy longevity.Expert opinion on therapeutic targets · 2024
    Article
  7. Aging-Related Mitochondrial Dysfunction Is Associated With Fibrosis in Benign Prostatic Hyperplasia.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024
    Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Aging related impairment of brain microvascular bioenergetics involves oxidative phosphorylation and glycolytic pathways.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022
    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

2 authors at 1 institution in 1 country.

Brandon J BerryDepartment of Laboratory Medicine and Pathology, University of Washington Medical Center, 1959 NE Pacific St, Seattle, WA, 98195, USA.
Matt KaeberleinDepartment of Laboratory Medicine and Pathology, University of Washington Medical Center, 1959 NE Pacific St, Seattle, WA, 98195, USA. kaeber@uw.edu.ORCID 0000-0002-1311-3421
University of Washington Medical Center · US

Funding

University of Washington Nathan Shock Center of Excellence in the Basic Biology of AgingP30AG013280 · NIA · UNIVERSITY OF WASHINGTON · PI Maitreya J Dunham · 1995 to 2026
$27.1M
Biological Mechanisms of Healthy Aging Training GrantT32AG066574 · NIA · UNIVERSITY OF WASHINGTON · PI David J. Marcinek, Jessica E Young · 2020 to 2026
$5.3M
Mechanisms of mitochondrial disease suppression in Ndufs4 knockout miceR01NS098329 · NINDS · UNIVERSITY OF WASHINGTON · PI KAEBERLEIN, MATT, VILLEN, JUDIT · 2017 to 2021
$2.4M
NIA NIH HHS P30 AG013280NIA NIH HHS T32 AG066574NINDS NIH HHS R01 NS098329
6 · The paper itself

Abstract

Mitochondria are organelles that provide energy to cells through ATP production. Mitochondrial dysfunction has long been postulated to mediate cellular declines that drive biological aging. Many well-characterized hallmarks of aging may involve underlying energetic defects that stem from loss of mitochondrial function with age. Why and how mitochondrial function declines with age is an open question and one that has been difficult to answer. Mitochondria are powered by an electrochemical gradient across the inner mitochondrial membrane known as the protonmotive force (PMF). This gradient decreases with age in several experimental models. However, it is unclear if a diminished PMF is a cause or a consequence of aging. Herein, we briefly review and define mitochondrial function, we summarize how PMF changes with age in several models, and we highlight recent studies that implicate PMF in aging biology. We also identify barriers that must be addressed for the field to progress. Emerging technology permits more precise in vivo study of mitochondria that will allow better understanding of cause and effect in metabolic models of aging. Once cause and effect can be discerned more precisely, energetics approaches to combat aging may be developed to prevent or reverse functional decline.

Indexed as

MitochondriaAMPKAutophagyMembrane potentialMetabolismmTOR

Identifiers

PMID33864592
PMCPMC8492883
OpenAlexW3152892086

What OpenQuestion holds

Textmetadata
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.