Evidence map›Paper›PMID 24818134›Full record

ReviewBioMed research international2014

Mitochondrial aging and age-related dysfunction of mitochondria.

Dimitry A Chistiakov, Igor A Sobenin, Victor V Revin, Alexander N Orekhov, Yuri V Bobryshev

Open access · hybridAbstract readReview
In one paragraph

Review in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 277 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
277citing papers in PubMed, 1 pooled it
10.1field-weighted citation impact, top 1% 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

277 citing papers in PubMed, 1 synthesis or guideline pooled it, 486 citations in OpenAlex.

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  11. Uncovering mitochondrial defects in photoreceptors opens therapeutic opportunities for Stargardt disease.Proceedings of the National Academy of Sciences of the United States of America · 2026
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217 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

5 authors at 4 institutions in 2 countries.

Dimitry A ChistiakovDepartment of Medical Nanobiotechnology, Pirogov Russian State Medical University, Moscow 117997, Russia.
Igor A SobeninLaboratory of Medical Genetics, Russian Cardiology Research and Production Complex, Moscow 121552, Russia ; Laboratory of Cellular Mechanisms of Atherogenesis, Institute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences, Moscow 125315, Russia.
Victor V RevinBiological Faculty, N.P. Ogaryov Mordovian State University, Saransk 430005, Russia.
Alexander N OrekhovLaboratory of Cellular Mechanisms of Atherogenesis, Institute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences, Moscow 125315, Russia ; Institute for Atherosclerosis Research, Skolkovo Innovative Center, Moscow 143025, Russia.
Yuri V BobryshevBiological Faculty, N.P. Ogaryov Mordovian State University, Saransk 430005, Russia ; Faculty of Medicine, University of New South Wales, Sydney, NSW 2052, Australia ; School of Medicine, University of Western Sydney, Campbelltown, NSW 2560, Australia.
Research Institute of General Pathology and Pathophysiology, the Russian Academy of Medical Sciences · RUNational Research Mordovia State University · RUPirogov Russian National Research Medical University · RUWestern Sydney University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Age-related changes in mitochondria are associated with decline in mitochondrial function. With advanced age, mitochondrial DNA volume, integrity and functionality decrease due to accumulation of mutations and oxidative damage induced by reactive oxygen species (ROS). In aged subjects, mitochondria are characterized by impaired function such as lowered oxidative capacity, reduced oxidative phosphorylation, decreased ATP production, significant increase in ROS generation, and diminished antioxidant defense. Mitochondrial biogenesis declines with age due to alterations in mitochondrial dynamics and inhibition of mitophagy, an autophagy process that removes dysfunctional mitochondria. Age-dependent abnormalities in mitochondrial quality control further weaken and impair mitochondrial function. In aged tissues, enhanced mitochondria-mediated apoptosis contributes to an increase in the percentage of apoptotic cells. However, implementation of strategies such as caloric restriction and regular physical training may delay mitochondrial aging and attenuate the age-related phenotype in humans.

Indexed as

Cellular SenescenceAgingAnimalsDNA, MitochondrialHumansMitochondriaMitochondrial DynamicsReactive Oxygen SpeciesDNA, MitochondrialReactive Oxygen Species

Identifiers

PMID24818134
PMCPMC4003832
OpenAlexW2010720463

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.