Evidence map›Paper›PMID 36369366›Full record

ReviewApoptosis : an international journal on programmed cell death2023

Regulation of autophagy of the heart in ischemia and reperfusion.

Sergey V Popov, Alexander V Mukhomedzyanov, Nikita S Voronkov, Ivan A Derkachev, Alla A Boshchenko, Feng Fu, Galina Z Sufianova, Maria S Khlestkina, Leonid N Maslov

Abstract readReview
PubMed Publisher
In one paragraph

Review in Apoptosis : an international journal on programmed cell death, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed, 3 pooled it
17.1field-weighted citation impact, top 1% 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

76 citing papers in PubMed, 3 syntheses or guidelines pooled it, 116 citations in OpenAlex.

  1. Pooled it
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  5. Review
  6. Healing mechanisms of Galectin-1 in the ischemic heart.Cell biochemistry and biophysics · 2026
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16 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

9 authors at 4 institutions in 2 countries.

Sergey V PopovCardiology Research Institute, Tomsk National Research Medical Centre, the Russian Academy of Sciences, Tomsk, Russia, 634012.
Alexander V MukhomedzyanovCardiology Research Institute, Tomsk National Research Medical Centre, the Russian Academy of Sciences, Tomsk, Russia, 634012.
Nikita S VoronkovCardiology Research Institute, Tomsk National Research Medical Centre, the Russian Academy of Sciences, Tomsk, Russia, 634012.
Ivan A DerkachevCardiology Research Institute, Tomsk National Research Medical Centre, the Russian Academy of Sciences, Tomsk, Russia, 634012.
Alla A BoshchenkoCardiology Research Institute, Tomsk National Research Medical Centre, the Russian Academy of Sciences, Tomsk, Russia, 634012.
Feng FuSchool of Basic Medicine, Fourth Military Medical University, No.169, West Changle Road, Xi'an, 710032, China.
Galina Z SufianovaTyumen State Medical University, Tyumen, Russia, 625023.
Maria S KhlestkinaTyumen State Medical University, Tyumen, Russia, 625023.
Leonid N MaslovCardiology Research Institute, Tomsk National Research Medical Centre, the Russian Academy of Sciences, Tomsk, Russia, 634012. maslov@cardio-tomsk.ru.
Tomsk National Research Medical Center · RUTyumen State Medical University · RUAir Force Medical University · CNRussian Academy of Sciences · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemia/reperfusion (I/R) of the heart leads to increased autophagic flux. Preconditioning stimulates autophagic flux by AMPK and PI3-kinase activation and mTOR inhibition. The cardioprotective effect of postconditioning is associated with activation of autophagy and increased activity of NO-synthase and AMPK. Oxidative stress stimulates autophagy in the heart during I/R. Superoxide radicals generated by NADPH-oxidase acts as a trigger for autophagy, possibly due to AMPK activation. There is reason to believe that AMPK, GSK-3β, PINK1, JNK, hexokinase II, MEK, PKCα, and ERK kinases stimulate autophagy, while mTOR, PKCδ, Akt, and PI3-kinase can inhibit autophagy in the heart during I/R. However, there is evidence that PI3-kinase could stimulate autophagy in ischemic preconditioning of the heart. It was found that transcription factors FoxO1, FoxO3, NF-κB, HIF-1α, TFEB, and Nrf-2 enhance autophagy in the heart in I/R. Transcriptional factors STAT1, STAT3, and p53 inhibit autophagy in I/R. MicroRNAs could stimulate and inhibit autophagy in the heart in I/R. Long noncoding RNAs regulate the viability and autophagy of cardiomyocytes in hypoxia/reoxygenation (H/R). Nitric oxide (NO) donors and endogenous NO could activate autophagy of cardiomyocytes. Activation of heme oxygenase-1 promotes cardiomyocyte tolerance to H/R and enhances autophagy. Hydrogen sulfide increases cardiac tolerance to I/R and inhibits apoptosis and autophagy via mTOR and PI3-kinase activation.

Indexed as

Myocardial Reperfusion InjurySignal TransductionAMP-Activated Protein KinasesApoptosisAutophagyGlycogen Synthase Kinase 3 betaHumansIschemiaMyocytes, CardiacPhosphatidylinositol 3-KinasesReperfusionTOR Serine-Threonine KinasesAMP-Activated Protein KinasesGlycogen Synthase Kinase 3 betaPhosphatidylinositol 3-KinasesTOR Serine-Threonine KinasesAutophagyHeartIschemia/reperfusionKinasesmicroRNAsReactive oxygen species

Identifiers

PMID36369366
OpenAlexW4308791124

What Socratic 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 Socratic graph.