Evidence map›Paper›PMID 35958017›Full record

ReviewOxidative medicine and cellular longevity2022

Mitochondrial Dysfunction and Cardiovascular Disease: Pathophysiology and Emerging Therapies.

Cosimo Andrea Stamerra, Paolo Di Giosia, Paolo Giorgini, Claudio Ferri, Vasily N Sukhorukov, Amirhossein Sahebkar

RetractedOpen access · hybridAbstract readReviewRetracted Publication
In one paragraph

Review in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
3.8field-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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
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  7. Observational
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  14. PMLife (Basel, Switzerland) · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 3 countries.

Cosimo Andrea StamerraUniversity of L'Aquila, Department of Life, Health and Environmental Sciences, Building Delta 6, San Salvatore Hospital, Via Vetoio, Coppito 67100 L'Aquila, Italy.
Paolo Di GiosiaUniversity of L'Aquila, Department of Life, Health and Environmental Sciences, Building Delta 6, San Salvatore Hospital, Via Vetoio, Coppito 67100 L'Aquila, Italy.
Paolo GiorginiUniversity of L'Aquila, Department of Life, Health and Environmental Sciences, Building Delta 6, San Salvatore Hospital, Via Vetoio, Coppito 67100 L'Aquila, Italy.
Claudio FerriUniversity of L'Aquila, Department of Life, Health and Environmental Sciences, Building Delta 6, San Salvatore Hospital, Via Vetoio, Coppito 67100 L'Aquila, Italy.
Vasily N SukhorukovInstitute for Atherosclerosis Research, Osennyaya Street 4-1-207, Moscow 121609, Russia.
Amirhossein SahebkarBiotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran.ORCID https://orcid.org/0000-0002-8656-1444
University of L'Aquila · ITInstitute for Atherosclerosis Research · RUMashhad University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria ensure the supply of cellular energy through the production of ATP via oxidative phosphorylation. The alteration of this process, called mitochondrial dysfunction, leads to a reduction in ATP and an increase in the production of reactive oxygen species (ROS). Mitochondrial dysfunction can be caused by mitochondrial/nuclear DNA mutations, or it can be secondary to pathological conditions such as cardiovascular disease, aging, and environmental stress. The use of therapies aimed at the prevention/correction of mitochondrial dysfunction, in the context of the specific treatment of cardiovascular diseases, is a topic of growing interest. In this context, the data are conflicting since preclinical studies are numerous, but there are no large randomized studies.

Indexed as

Cardiovascular DiseasesAdenosine TriphosphateDNA, MitochondrialHumansMitochondriaOxidative PhosphorylationOxidative StressReactive Oxygen SpeciesAdenosine TriphosphateDNA, MitochondrialReactive Oxygen Species

Identifiers

PMID35958017
PMCPMC9363184
OpenAlexW4289519687

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.