Evidence map›Paper›PMID 35145250›Full record

ReviewNature reviews. Endocrinology2022

Mitochondrial and metabolic dysfunction in ageing and age-related diseases.

João A Amorim, Giuseppe Coppotelli, Anabela P Rolo, Carlos M Palmeira, Jaime M Ross, David A Sinclair

Abstract readReview
In one paragraph

Review in Nature reviews. Endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 541 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
541citing papers in PubMed, 1 pooled it
–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

541 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  8. Mitochondrial dysfunction in urologic disease.Prostate cancer and prostatic diseases · 2026
    Review
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481 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

6 authors.

João A AmorimDepartment of Genetics, Blavatnik Institute, Paul F. Glenn Center for the Biology of Aging, Harvard Medical School, Boston, MA, USA.ORCID http://orcid.org/0000-0002-7720-6264
Giuseppe CoppotelliDepartment of Genetics, Blavatnik Institute, Paul F. Glenn Center for the Biology of Aging, Harvard Medical School, Boston, MA, USA.ORCID http://orcid.org/0000-0002-6067-001X
Anabela P RoloCenter for Neurosciences and Cell Biology of the University of Coimbra, Coimbra, Portugal.ORCID http://orcid.org/0000-0003-3535-9630
Carlos M PalmeiraCenter for Neurosciences and Cell Biology of the University of Coimbra, Coimbra, Portugal.
Jaime M RossDepartment of Genetics, Blavatnik Institute, Paul F. Glenn Center for the Biology of Aging, Harvard Medical School, Boston, MA, USA.ORCID http://orcid.org/0000-0002-3879-4817
David A SinclairDepartment of Genetics, Blavatnik Institute, Paul F. Glenn Center for the Biology of Aging, Harvard Medical School, Boston, MA, USA. david_sinclair@hms.harvard.edu.ORCID http://orcid.org/0000-0002-9936-436X

Funding

Elucidating mechanisms of SIRT1 activationR01DK100263 · NIDDK · HARVARD MEDICAL SCHOOL · PI SINCLAIR, DAVID A. · 2016 to 2020
$2.5M
SIRT as a regulator of health and lifespan of mammalsR01AG028730 · NIA · HARVARD MEDICAL SCHOOL · PI SINCLAIR, DAVID A. · 2007 to 2011
$1.7M
The role of epigenetics in age-related cognitive decline and Alzheimer's diseaseR00AG055683 · NIA · UNIVERSITY OF RHODE ISLAND · PI ROSS, JAIME MARIE · 2020 to 2022
$747k
NIA NIH HHS R00 AG055683NIA NIH HHS R01 AG028730NIDDK NIH HHS R01 DK100263
6 · The paper itself

Abstract

Organismal ageing is accompanied by progressive loss of cellular function and systemic deterioration of multiple tissues, leading to impaired function and increased vulnerability to death. Mitochondria have become recognized not merely as being energy suppliers but also as having an essential role in the development of diseases associated with ageing, such as neurodegenerative and cardiovascular diseases. A growing body of evidence suggests that ageing and age-related diseases are tightly related to an energy supply and demand imbalance, which might be alleviated by a variety of interventions, including physical activity and calorie restriction, as well as naturally occurring molecules targeting conserved longevity pathways. Here, we review key historical advances and progress from the past few years in our understanding of the role of mitochondria in ageing and age-related metabolic diseases. We also highlight emerging scientific innovations using mitochondria-targeted therapeutic approaches.

Indexed as

AgingMetabolic DiseasesCaloric RestrictionEnergy MetabolismHumansMitochondria

Identifiers

PMID35145250
PMCPMC9059418

What OpenQuestion holds

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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.