Evidence map›Paper›PMID 35021300›Full record

ReviewThe world journal of men's health2022

The Role of Mitochondrial Dynamic Dysfunction in Age-Associated Type 2 Diabetes.

Teresa Vezza, Pedro Díaz-Pozo, Francisco Canet, Aranzazu M de Marañón, Zaida Abad-Jiménez, Celia García-Gargallo, Ildefonso Roldan, Eva Solá, Celia Bañuls, Sandra López-Domènech and 2 more

Open access · diamondAbstract readReview
In one paragraph

Review in The world journal of men's health, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.2field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 48 citations in OpenAlex.

  1. PMF proteins mediate mitochondrial fusion in Arabidopsis.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  9. Mitochondrial Dysfunction in Diabetes: Shedding Light on a Widespread Oversight.Pathophysiology : the official journal of the International Society for Pathophysiology · 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

12 authors at 3 institutions in 1 country.

Teresa VezzaService of Endocrinology and Nutrition, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain.ORCID https://orcid.org/0000-0002-9780-0180
Pedro Díaz-PozoService of Endocrinology and Nutrition, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain.ORCID https://orcid.org/0000-0001-5241-5994
Francisco CanetService of Endocrinology and Nutrition, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain.ORCID https://orcid.org/0000-0002-6626-2762
Aranzazu M de MarañónService of Endocrinology and Nutrition, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain.ORCID https://orcid.org/0000-0002-4153-0396
Zaida Abad-JiménezService of Endocrinology and Nutrition, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain.ORCID https://orcid.org/0000-0001-6258-4724
Celia García-GargalloService of Endocrinology and Nutrition, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain.ORCID https://orcid.org/0000-0003-4298-2017
Ildefonso RoldanService of Cardiology, University Hospital Doctor Peset, FISABIO, Valencia, Spain.ORCID https://orcid.org/0000-0002-3031-0785
Eva SoláService of Endocrinology and Nutrition, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain.ORCID https://orcid.org/0000-0003-2721-6920
Celia BañulsService of Endocrinology and Nutrition, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain. celia.banuls@uv.es.ORCID https://orcid.org/0000-0001-8077-7642
Sandra López-DomènechService of Endocrinology and Nutrition, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain.ORCID https://orcid.org/0000-0003-2067-9308
Milagros RochaService of Endocrinology and Nutrition, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain.ORCID https://orcid.org/0000-0003-2923-6546
Víctor M VíctorService of Endocrinology and Nutrition, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain.ORCID https://orcid.org/0000-0002-3027-3945
Fundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunitat Valenciana · ESHospital Universitario Doctor Peset · ESUniversitat de València · ES

Funding

Carlos III Health Institute CIBERehd CB06/04/0071Carlos III Health Institute PI19/00838Carlos III Health Institute PI19/0437European Regional Development FundFISABIO UGP15-220Menarini S.AMinistry of Education of the Valencian Regional Government PROMETEO/2019/027
6 · The paper itself

Abstract

Mitochondrial dynamics, such as fusion and fission, play a critical role in maintaining cellular metabolic homeostasis. The molecular mechanisms underlying these processes include fusion proteins (Mitofusin 1 [MFN1], Mitofusin 2 [MFN2], and optic atrophy 1 [OPA1]) and fission mediators (mitochondrial fission 1 [FIS1] and dynamin-related protein 1 [DRP1]), which interact with each other to ensure mitochondrial quality control. Interestingly, defects in these proteins can lead to the loss of mitochondrial DNA (mtDNA) integrity, impairment of mitochondrial function, a severe alteration of mitochondrial morphology, and eventually cell death. Emerging evidence has revealed a causal relationship between dysregulation of mitochondria dynamics and age-associated type 2 diabetes, a metabolic disease whose rates have reached an alarming epidemic-like level with the majority of cases (59%) recorded in men aged 65 and over. In this sense, fragmentation of mitochondrial networks is often associated with defects in cellular energy production and increased apoptosis, leading, in turn, to excessive reactive oxygen species release, mitochondrial dysfunction, and metabolic alterations, which can ultimately contribute to β-cell dysfunction and insulin resistance. The present review discusses the processes of mitochondrial fusion and fission and their dysfunction in type 2 diabetes, with special attention given to the therapeutic potential of targeting mitochondrial dynamics in this complex metabolic disorder.

Indexed as

AgingMenMitochondriaType 2 diabetes

Identifiers

PMID35021300
PMCPMC9253806
OpenAlexW4205288533

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.