Evidence map›Paper›PMID 40149969›Full record

ReviewBiomolecules2025

The Balance of MFN2 and OPA1 in Mitochondrial Dynamics, Cellular Homeostasis, and Disease.

Paola Zanfardino, Alessandro Amati, Mirko Perrone, Vittoria Petruzzella

Abstract readReview
In one paragraph

Review in Biomolecules, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing 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

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

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3 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.

Paola ZanfardinoDepartment of Translational Biomedicine and Neurosciences (DiBraiN), University of Bari Aldo Moro, Piazza Giulio Cesare, 70124 Bari, Italy.ORCID 0000-0002-8297-5041
Alessandro AmatiDepartment of Translational Biomedicine and Neurosciences (DiBraiN), University of Bari Aldo Moro, Piazza Giulio Cesare, 70124 Bari, Italy.ORCID 0000-0002-4995-7239
Mirko PerroneDepartment of Translational Biomedicine and Neurosciences (DiBraiN), University of Bari Aldo Moro, Piazza Giulio Cesare, 70124 Bari, Italy.ORCID 0009-0001-8212-6541
Vittoria PetruzzellaDepartment of Translational Biomedicine and Neurosciences (DiBraiN), University of Bari Aldo Moro, Piazza Giulio Cesare, 70124 Bari, Italy.ORCID 0000-0001-8771-6033

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial dynamics, governed by fusion and fission, are crucial for maintaining cellular homeostasis, energy production, and stress adaptation. MFN2 and OPA1, key regulators of mitochondrial fusion, play essential roles beyond their structural functions, influencing bioenergetics, intracellular signaling, and quality control mechanisms such as mitophagy. Disruptions in these processes, often caused by MFN2 or OPA1 mutations, are linked to neurodegenerative diseases like Charcot-Marie-Tooth disease type 2A (CMT2A) and autosomal dominant optic atrophy (ADOA). This review explores the molecular mechanisms underlying mitochondrial fusion, the impact of MFN2 and OPA1 dysfunction on oxidative phosphorylation and autophagy, and their role in disease progression. Additionally, we discuss the divergent cellular responses to MFN2 and OPA1 mutations, particularly in terms of proliferation, senescence, and metabolic signaling. Finally, we highlight emerging therapeutic strategies to restore mitochondrial integrity, including mTOR modulation and autophagy-targeted approaches, with potential implications for neurodegenerative disorders.

Indexed as

Charcot-Marie-Tooth DiseaseGTP PhosphohydrolasesMitochondrial DynamicsMitochondrial ProteinsAnimalsAutophagyHomeostasisHumansMitochondriaMutationOptic Atrophy, Autosomal DominantGTP PhosphohydrolasesMFN2 protein, humanMitochondrial ProteinsOPA1 protein, humanautophagymitochondriamitochondrial dynamicsmitophagymTOR signalingneurodegenerative diseasesoxidative phosphorylationproliferationsenescence

Identifiers

PMID40149969
PMCPMC11940761

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.