Evidence map›Paper›PMID 32738358›Full record

ReviewMitochondrion2020

Mitochondrial pathways in human health and aging.

Rebecca Bornstein, Brenda Gonzalez, Simon C Johnson

Open access · greenAbstract readReview
In one paragraph

Review in Mitochondrion, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Prenatal Alcohol Exposure and Mitochondrial Function in the Brain.Advances in experimental medicine and biology · 2026
    Review
  6. Review
  7. Thermogenic Adipose ADH5 Counteracts Age-related Metabolic Decline.bioRxiv : the preprint server for biology · 2025
    Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Antiphotoaging effects of solvent fractions isolated fromBiochemistry and biophysics reports · 2024
    Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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

3 authors at 2 institutions in 1 country.

Rebecca BornsteinDepartment of Pathology, University of Washington, Seattle, WA, USA.
Brenda GonzalezDepartment of Genetics, Albert Einstein College of Medicine, Bronx, NY, USA.
Simon C JohnsonDepartment of Neurology, University of Washington, Seattle, WA, USA; Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, WA, USA; Center for Integrative Brain Research, Seattle Children's Research Institute, Seattle, WA, USA. Electronic address: simoncj@uw.edu.
University of Washington · USAlbert Einstein College of Medicine · US

Funding

Molecular Medicine Training ProgramT32GM095421 · NIGMS · UNIVERSITY OF WASHINGTON · PI HAWN, THOMAS R, LILES, W. CONRAD · 2011 to 2020
$1.6M
The role of mTOR in mitochondrial encephalopathyR00GM126147 · NIGMS · SEATTLE CHILDREN'S HOSPITAL · PI JOHNSON, SIMON C · 2019 to 2021
$747k
The role of mTOR in mitochondrial encephalopathyK99GM126147 · NIGMS · SEATTLE CHILDREN'S HOSPITAL · PI JOHNSON, SIMON C · 2017 to 2018
$180k
NIGMS NIH HHS K99 GM126147NIGMS NIH HHS R00 GM126147NIGMS NIH HHS T32 GM095421
6 · The paper itself

Abstract

Mitochondria are eukaryotic organelles known best for their roles in energy production and metabolism. While often thought of as simply the 'powerhouse of the cell,' these organelles participate in a variety of critical cellular processes including reactive oxygen species (ROS) production, regulation of programmed cell death, modulation of inter- and intracellular nutrient signaling pathways, and maintenance of cellular proteostasis. Disrupted mitochondrial function is a hallmark of eukaryotic aging, and mitochondrial dysfunction has been reported to play a role in many aging-related diseases. While mitochondria are major players in human diseases, significant questions remain regarding their precise mechanistic role. In this review, we detail mechanisms by which mitochondrial dysfunction participate in disease and aging based on findings from model organisms and human genetics studies.

Indexed as

AgingApoptosisEnergy MetabolismHumansMitochondriaOxidative StressProteostasisReactive Oxygen SpeciesReactive Oxygen Species

Identifiers

PMID32738358
PMCPMC7508824
OpenAlexW3046073734

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.