Evidence map›Paper›PMID 31667999›Full record

ReviewEMBO reports2019

Causal roles of mitochondrial dynamics in longevity and healthy aging.

Arpit Sharma, Hannah J Smith, Pallas Yao, William B Mair

Open access · bronzeAbstract readReview
In one paragraph

Review in EMBO reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
129citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 2% 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

129 citing papers in PubMed, 1 synthesis or guideline pooled it, 209 citations in OpenAlex.

  1. The Role of Estrogen in Mitochondrial Disease.Cellular and molecular neurobiology · 2025
    Pooled it
  2. Article
  3. Review
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  17. Aging impairs peroxisome biogenesis in human B cells.The journals of gerontology. Series A, Biological sciences and medical sciences · 2026
    Article
  18. Article
  19. Article
  20. Article

69 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Arpit SharmaDepartment of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Hannah J SmithDepartment of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Pallas YaoDepartment of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
William B MairDepartment of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, MA, USA.ORCID 0000-0002-0661-1342
Harvard University · US

Funding

Training Program in Molecular and Integrative Physiological SciencesT32HL007118 · NHLBI · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI LU, QUAN · 1985 to 2025
$14.3M
NHLBI NIH HHS T32 HL007118
6 · The paper itself

Abstract

Mitochondria are organized in the cell in the form of a dynamic, interconnected network. Mitochondrial dynamics, regulated by mitochondrial fission, fusion, and trafficking, ensure restructuring of this complex reticulum in response to nutrient availability, molecular signals, and cellular stress. Aberrant mitochondrial structures have long been observed in aging and age-related diseases indicating that mitochondrial dynamics are compromised as cells age. However, the specific mechanisms by which aging affects mitochondrial dynamics and whether these changes are causally or casually associated with cellular and organismal aging is not clear. Here, we review recent studies that show specifically how mitochondrial fission, fusion, and trafficking are altered with age. We discuss factors that change with age to directly or indirectly influence mitochondrial dynamics while examining causal roles for altered mitochondrial dynamics in healthy aging and underlying functional outputs that might affect longevity. Lastly, we propose that altered mitochondrial dynamics might not just be a passive consequence of aging but might constitute an adaptive mechanism to mitigate age-dependent cellular impairments and might be targeted to increase longevity and promote healthy aging.

Indexed as

AgingAMP-Activated Protein KinasesAnimalsCellular SenescenceHealthy AgingHost Microbial InteractionsHumansInsulinLongevityMicrobiotaMitochondrial DynamicsModels, BiologicalOrganellesSignal TransductionSirtuinsSomatomedinsAMP-Activated Protein KinasesInsulinSirtuinsSomatomedinsTOR Serine-Threonine Kinasesagingfissionfusionmitochondriamitochondrial dynamics

Identifiers

PMID31667999
PMCPMC6893295
OpenAlexW2982479733

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.