Evidence map›Paper›PMID 33741252›Full record

ArticleSeminars in cell & developmental biology2021

Aging: All roads lead to mitochondria.

Jyung Mean Son, Changhan Lee

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Seminars in cell & developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
5.0field-weighted citation impact, top 3% 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

46 citing papers in PubMed, 82 citations in OpenAlex.

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  6. Mitochondria in focus: From structure and function to their role in human diseases. A review.Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia · 2025
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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 2 institutions in 2 countries.

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, USA; USC Norris Comprehensive Cancer Center, Los Angeles, CA 90089, USA; Biomedical Sciences, Graduate School, Ajou University, Suwon 16499, South Korea.
Ajou University · KRUniversity of Southern California · US

Funding

Use of viral-vectors for studying effects of chronic inflammation on executive functionR01AG052258 · NIA · UNIVERSITY OF FLORIDA · PI FOSTER, THOMAS C · 2016 to 2020
$1.9M
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 AG052258NIA NIH HHS R01 AG052558NIGMS NIH HHS R01 GM136837
6 · The paper itself

Abstract

Mitochondria were described as early as 1890 as ubiquitous intracellular structures by Ernster and Schatz (1981) [1]. Since then, the accretion of knowledge in the past century has revealed much of the molecular details of mitochondria, ranging from mitochondrial origin, structure, metabolism, genetics, and signaling, and their implications in health and disease. We now know that mitochondria are remarkably multifunctional and deeply intertwined with many vital cellular processes. They are quasi-self organelles that still possess remnants of its bacterial ancestry, including an independent genome. The mitochondrial free radical theory of aging (MFRTA), which postulated that aging is a product of oxidative damage to mitochondrial DNA, provided a conceptual framework that put mitochondria on the map of aging research. However, several studies have more recently challenged the general validity of the theory, favoring novel ideas based on emerging evidence to understand how mitochondria contribute to aging and age-related diseases. One prominent topic of investigation lies on the fact that mitochondria are not only production sites for bioenergetics and macromolecules, but also regulatory hubs that communicate and coordinate many vital physiological processes at the cellular and organismal level. The bi-directional communication and coordination between the co-evolved mitochondrial and nuclear genomes is especially interesting in terms of cellular regulation. Mitochondria are dynamic and adaptive, rendering their function sensitive to cellular context. Tissues with high energy demands, such as the brain, seem to be uniquely affected by age-dependent mitochondrial dysfunction, providing a foundation for the development of novel mitochondrial-based therapeutics and diagnostics.

Indexed as

AgingAnimalsHumansMiceMitochondriaRatsAgingCommunicationGenomic instabilityImmunityInflammationLongevityMitochondriaMitochondrial-derived peptidesMitonuclearOxidative stress

Identifiers

PMID33741252
PMCPMC9774040
OpenAlexW3137358241

What OpenQuestion 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 OpenQuestion graph.