Evidence map›Paper›PMID 36107370›Full record

ReviewMolecular biology reports2022

Protective and deleterious effects of autophagy in the setting of myocardial ischemia/reperfusion injury: an overview.

Behnaz Mokhtari, Reza Badalzadeh

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular biology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
4.8field-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

8 citing papers in PubMed, 33 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

Behnaz MokhtariMolecular Medicine Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.ORCID https://orcid.org/0000-0002-3355-9869
Reza BadalzadehDrug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. badalzadehr@tbzmed.ac.ir.ORCID http://orcid.org/0000-0002-8092-7820
Tabriz University of Medical Sciences · IR

Funding

Drug Applied Research Center, Tabriz University of Medical Sciences IR.TBZMED.VCR.REC.1400.468
6 · The paper itself

Abstract

introductionAutophagy is known as a conserved mechanism in order to preserve cell survival under various stress conditions via maintaining cellular homeostasis. Although autophagy is active in the heart at baseline and plays a critical role in cell survival, inappropriate activation of autophagy following ischemia/reperfusion (I/R) injury leads to cell death. MAIN TEXT: The distinct functions of autophagy in myocardial I/R injury condition have been examined in numerous studies, however, contradicting results have been achieved in this field. These studies have documented that autophagy acts as a double-edged sword in myocardial I/R injury. Clarifying the exact role of autophagy in determining the health or death of cardiomyocytes under I/R injury is very helpful to achieve better cardioprotection in prospective clinical studies. Thus, autophagy may be an interesting target for the treatment or prevention of myocardial I/R injury. But before considering this matter, it is necessary to address the gaps in our knowledge about the complex role of autophagy in myocardial I/R injury.

conclusionIn this review, by providing updated data about the role of autophagy in the heart during ischemia and reperfusion, we tried to provide more insights in this context and encourage scientists to pay special attention towards manipulating autophagy as an intriguing and powerful approach in cardioprotection.

Indexed as

Myocardial Reperfusion InjuryAutophagyCell SurvivalHumansMyocytes, CardiacProspective StudiesCardioprotectionDeleterious autophagyMyocardial ischemiaMyocardial reperfusionProtective autophagy

Identifiers

PMID36107370
OpenAlexW4295904272

What OpenQuestion holds

Textmetadata
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.