Evidence map›Paper›PMID 39015222›Full record

ReviewFrontiers in physiology2024

Mitochondrial dysfunction and its association with age-related disorders.

Indumathi Somasundaram, Samatha M Jain, Marcel Blot-Chabaud, Surajit Pathak, Antara Banerjee, Sonali Rawat, Neeta Raj Sharma, Asim K Duttaroy

Abstract readReview
In one paragraph

Review in Frontiers in physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing 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

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

  1. The Role of Estrogen in Mitochondrial Disease.Cellular and molecular neurobiology · 2025
    Pooled it
  2. Trial
  3. Article
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  5. Cutaneous Aging in Skin of Color: A Narrative Review.American journal of clinical dermatology · 2026
    Review
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  8. Article
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  20. Lysosomal homeostasis at the crossroads of neurodegeneration.The Journal of clinical investigation · 2026
    Review

1 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

8 authors.

Indumathi SomasundaramBiotechnology Engineering, Kolhapur Institute of Technology's College of Engineering, Kolhapur, India.
Samatha M JainDepartment of Biotechnology, Faculty of Allied Health Sciences, Chettinad Hospital and Research Institute, Chettinad Academy of Research and Education, Chennai, India.
Marcel Blot-ChabaudC2VN, Aix-Marseille University, Marseille, France.
Surajit PathakDepartment of Biotechnology, Faculty of Allied Health Sciences, Chettinad Hospital and Research Institute, Chettinad Academy of Research and Education, Chennai, India.
Antara BanerjeeDepartment of Biotechnology, Faculty of Allied Health Sciences, Chettinad Hospital and Research Institute, Chettinad Academy of Research and Education, Chennai, India.
Sonali RawatStem Cell Facility, DBT-Centre of Excellence for Stem Cell Research, All India Institute of Medical Sciences, New Delhi, India.
Neeta Raj SharmaSchool of Bioengineering and Biosciences, Lovely Professional University, Phagwara, India.
Asim K DuttaroyDepartment of Nutrition, Faculty of Medicine, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging is a complex process that features a functional decline in many organelles. Various factors influence the aging process, such as chromosomal abnormalities, epigenetic changes, telomere shortening, oxidative stress, and mitochondrial dysfunction. Mitochondrial dysfunction significantly impacts aging because mitochondria regulate cellular energy, oxidative balance, and calcium levels. Mitochondrial integrity is maintained by mitophagy, which helps maintain cellular homeostasis, prevents ROS production, and protects against mtDNA damage. However, increased calcium uptake and oxidative stress can disrupt mitochondrial membrane potential and permeability, leading to the apoptotic cascade. This disruption causes increased production of free radicals, leading to oxidative modification and accumulation of mitochondrial DNA mutations, which contribute to cellular dysfunction and aging. Mitochondrial dysfunction, resulting from structural and functional changes, is linked to age-related degenerative diseases. This review focuses on mitochondrial dysfunction, its implications in aging and age-related disorders, and potential anti-aging strategies through targeting mitochondrial dysfunction.

Indexed as

chromosomal aberrationsmitochondrial DNAmitochondrial dysfunctionmitophagyROS production

Identifiers

PMID39015222
PMCPMC11250148

What Socratic 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 Socratic graph.