Evidence map›Paper›PMID 32245255›Full record

ReviewInternational journal of molecular sciences2020

The Role of Reactive Oxygen Species in the Life Cycle of the Mitochondrion.

Paola Venditti, Sergio Di Meo

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
6.3field-weighted citation impact, top 2% 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

61 citing papers in PubMed, 141 citations in OpenAlex.

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  20. Protein Nitration in Patients with Mitochondrial Diseases.Antioxidants (Basel, Switzerland) · 2025
    Article

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

2 authors at 1 institution in 1 country.

Paola VendittiDipartimento di Biologia, Università di Napoli Federico II, Complesso Universitario Monte Sant'Angelo, Via Cinthia, I-80126 Napoli, Italy.
Sergio Di MeoDipartimento di Biologia, Università di Napoli Federico II, Complesso Universitario Monte Sant'Angelo, Via Cinthia, I-80126 Napoli, Italy.
Istituto Nazionale di Fisica Nucleare, Sezione di Napoli · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Currently, it is known that, in living systems, free radicals and other reactive oxygen and nitrogen species play a double role, because they can cause oxidative damage and tissue dysfunction and serve as molecular signals activating stress responses that are beneficial to the organism. It is also known that mitochondria, because of their capacity to produce free radicals, play a major role in tissue oxidative damage and dysfunction and provide protection against excessive tissue dysfunction through several mechanisms, including the stimulation of permeability transition pore opening. This process leads to mitoptosis and mitophagy, two sequential processes that are a universal route of elimination of dysfunctional mitochondria and is essential to protect cells from the harm due to mitochondrial disordered metabolism. To date, there is significant evidence not only that the above processes are induced by enhanced reactive oxygen species (ROS) production, but also that such production is involved in the other phases of the mitochondrial life cycle. Accumulating evidence also suggests that these effects are mediated through the regulation of the expression and the activity of proteins that are engaged in processes such as genesis, fission, fusion, and removal of mitochondria. This review provides an account of the developments of the knowledge on the dynamics of the mitochondrial population, examining the mechanisms governing their genesis, life, and death, and elucidating the role played by free radicals in such processes.

Indexed as

AMP-Activated Protein Kinase KinasesAnimalsHumansMechanistic Target of Rapamycin Complex 1MitochondriaMitochondrial DynamicsMitophagyNF-E2-Related Factor 2Oxidative StressProtein KinasesReactive Oxygen SpeciesSignal TransductionTranscription FactorsAMP-Activated Protein Kinase KinasesMechanistic Target of Rapamycin Complex 1NF-E2-Related Factor 2peroxisome-proliferator-activated receptor-gamma coactivator-1Protein KinasesReactive Oxygen SpeciesTranscription Factorsmitochondrial fissionmitochondrial fusionmitochondrial turnovermitophagyNrf2PGC-1ROStransition pore

Identifiers

PMID32245255
PMCPMC7139706
OpenAlexW3012285865

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.