Evidence map›Paper›PMID 30545443›Full record

ReviewBMB reports2019

Mitochondria: multifaceted regulators of aging.

Jyung Mean Son, Changhan Lee

Abstract readReview
PubMed Full text at PMC
In one paragraph

Review in BMB reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
–field-weighted citation impact
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

40 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
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.

Jyung Mean SonLeonard Davis School of Gerontology, University of Southern California, Los Angeles, CA 90089, USA.
Changhan LeeLeonard Davis School of Gerontology, University of Southern California, Los Angeles, CA 90089; USC Norris Comprehensive Cancer Center, Los Angeles, CA 90089, USA; Biomedical Science, Graduate School, Ajou University, Suwon 16499, Korea.

Funding

Novel Regulators of Aging Metabolism Encoded in the Mitochondrial GenomeR01AG052558 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LEE, CHANGHAN · 2016 to 2020
$1.8M
Regulation of Cellular Proliferation by Novel Mitochondrial-Encoded Tumor SuppressorsR01GM136837 · NIGMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LEE, CHANGHAN · 2020 to 2023
$1.5M
NIA NIH HHS R01 AG052558NIGMS NIH HHS R01 GM136837
6 · The paper itself

Abstract

Aging is accompanied by a time-dependent progressive deterioration of multiple factors of the cellular system. The past several decades have witnessed major leaps in our understanding of the biological mechanisms of aging using dietary, genetic, pharmacological, and physical interventions. Metabolic processes, including nutrient sensing pathways and mitochondrial function, have emerged as prominent regulators of aging. Mitochondria have been considered to play a key role largely due to their production of reactive oxygen species (ROS), resulting in DNA damage that accumulates over time and ultimately causes cellular failure. This theory, known as the mitochondrial free radical theory of aging (MFRTA), was favored by the aging field, but increasing inconsistent evidence has led to criticism and rejection of this idea. However, MFRTA should not be hastily rejected in its entirety because we now understand that ROS is not simply an undesired toxic metabolic byproduct, but also an important signaling molecule that is vital to cellular fitness. Notably, mitochondrial function, a term traditionally referred to bioenergetics and apoptosis, has since expanded considerably. It encompasses numerous other key biological processes, including the following: (i) complex metabolic processes, (ii) intracellular and endocrine signaling/communication, and (iii) immunity/inflammation. Here, we will discuss shortcomings of previous concepts regarding mitochondria in aging and their emerging roles based on recent advances. We will also discuss how the mitochondrial genome integrates with major theories on the evolution of aging. [BMB Reports 2019; 52(1): 13-23].

Indexed as

AgingAnimalsApoptosisDNA DamageDNA, MitochondrialFree RadicalsHumansMitochondriaOxidative StressReactive Oxygen SpeciesDNA, MitochondrialFree RadicalsReactive Oxygen Species

Identifiers

PMID30545443
PMCPMC6386233

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.