Evidence map›Paper›PMID 36232693›Full record

ReviewInternational journal of molecular sciences2022

Mitochondrial DNA Repair in Neurodegenerative Diseases and Ageing.

Veronica Bazzani, Mara Equisoain Redin, Joshua McHale, Lorena Perrone, Carlo Vascotto

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
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  16. Role ofFrontiers in pharmacology · 2025
    Review
  17. Review
  18. Novel Techniques for Mapping DNA Damage and Repair in the Brain.International journal of molecular sciences · 2024
    Review
  19. Ovarian aging: energy metabolism of oocytes.Journal of ovarian research · 2024
    Review
  20. Article
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 2 institutions in 2 countries.

Veronica BazzaniDepartment of Medicine, University of Udine, 33100 Udine, Italy.ORCID 0000-0002-6900-1808
Mara Equisoain RedinDepartment of Medicine, University of Udine, 33100 Udine, Italy.
Joshua McHaleDepartment of Medicine, University of Udine, 33100 Udine, Italy.ORCID 0000-0003-0435-7122
Lorena PerroneDepartment of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, 80100 Naples, Italy.
Carlo VascottoDepartment of Medicine, University of Udine, 33100 Udine, Italy.ORCID 0000-0003-4431-029X
University of Udine · ITUniversity of Campania "Luigi Vanvitelli" · IT

Funding

European Union Marie Skłodowska-Curie grant agreement no. 956070
6 · The paper itself

Abstract

Mitochondria are the only organelles, along with the nucleus, that have their own DNA. Mitochondrial DNA (mtDNA) is a double-stranded circular molecule of ~16.5 kbp that can exist in multiple copies within the organelle. Both strands are translated and encode for 22 tRNAs, 2 rRNAs, and 13 proteins. mtDNA molecules are anchored to the inner mitochondrial membrane and, in association with proteins, form a structure called nucleoid, which exerts a structural and protective function. Indeed, mitochondria have evolved mechanisms necessary to protect their DNA from chemical and physical lesions such as DNA repair pathways similar to those present in the nucleus. However, there are mitochondria-specific mechanisms such as rapid mtDNA turnover, fission, fusion, and mitophagy. Nevertheless, mtDNA mutations may be abundant in somatic tissue due mainly to the proximity of the mtDNA to the oxidative phosphorylation (OXPHOS) system and, consequently, to the reactive oxygen species (ROS) formed during ATP production. In this review, we summarise the most common types of mtDNA lesions and mitochondria repair mechanisms. The second part of the review focuses on the physiological role of mtDNA damage in ageing and the effect of mtDNA mutations in neurodegenerative disorders such as Alzheimer's and Parkinson's disease. Considering the central role of mitochondria in maintaining cellular homeostasis, the analysis of mitochondrial function is a central point for developing personalised medicine.

Indexed as

Mitochondrial DiseasesNeurodegenerative DiseasesAdenosine TriphosphateDNA DamageDNA, MitochondrialDNA RepairHumansReactive Oxygen SpeciesAdenosine TriphosphateDNA, MitochondrialReactive Oxygen SpeciesAlzheimer’s diseaseDNA damageDNA repair pathwaysmitochondrianeurodegenerative diseasesParkinson’s disease

Identifiers

PMID36232693
PMCPMC9569545
OpenAlexW4297539133

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.