Evidence map›Paper›PMID 30729392›Full record

ReviewJournal of physiology and biochemistry2019

Diabetes abolish cardioprotective effects of remote ischemic conditioning: evidences and possible mechanisms.

Sakshi Tyagi, Nirmal Singh, Jasleen Kaur Virdi, Amteshwar Singh Jaggi

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of physiology and biochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 2 pooled it
4.2field-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

29 citing papers in PubMed, 2 syntheses or guidelines pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Remote ischemic conditioning for stroke: A critical systematic review.International journal of stroke : official journal of the International Stroke Society · 2024
    Pooled it
  3. Trial
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Proteomics of the heart.Physiological reviews · 2024
    Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Regulation of autophagy of the heart in ischemia and reperfusion.Apoptosis : an international journal on programmed cell death · 2023
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Ischemic tolerance - blessing or curse.Physiological research · 2021
    Review
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

4 authors at 1 institution in 1 country.

Sakshi TyagiDepartment of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, 147002, India.
Nirmal SinghDepartment of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, 147002, India.
Jasleen Kaur VirdiDepartment of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, 147002, India.
Amteshwar Singh JaggiDepartment of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, 147002, India. amteshwarjaggi@pbi.ac.in.
Punjabi University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes mellitus significantly hampers the development of cardioprotective response to remote pre/post/perconditioning stimuli by impairing the activation of cardioprotective signaling pathways. Among the different pathways, the impairment in O-linked β-N-acetylglucosamine (O-GlcNAc) signaling and release of cardioprotective humoral factor may contribute in attenuating remote preconditioning-induced cardioprotection. Moreover, the failure to phosphorylate extracellular signal related kinase (ERK), phosphoinositide-3-kinase (PI3K), and AKT along with up-regulation of mechanistic target of rapamycin (mTOR) and decrease in autophagy may also attenuate remote preconditioning-induced cardioprotection. Remote perconditioning stimulus also fails to phosphorylate AKT kinase in diabetic heart. In addition, diabetes may increase the oxidative stress, reactive oxygen species (ROS) production, decrease the beclin expression, and inhibit autophagy to attenuate remote perconditioning-induced cardioprotection. Moreover, diabetes-induced increase in the Rho-associated kinase (ROCK) activity, decrease in the arginase activity, and reduction in nitric oxide (NO) bioavailability may also contribute in decreasing remote perconditioning-induced cardioprotection. Diabetes may reduce the phosphorylation of adenosine 5'-monophosphate activated protein kinase (AMPKα) and increase the phosphorylation of mTOR to attenuate cardioprotection of remote postconditioning. The present review describes the role of diabetes in attenuating remote ischemic conditioning-induced cardioprotection along with the possible mechanisms.

Indexed as

Gene Expression RegulationIschemic Preconditioning, MyocardialSignal TransductionAcetylglucosamineAMP-Activated Protein KinasesAnimalsArginaseAutophagyBeclin-1Diabetes Mellitus, Type 2HumansMyocardial InfarctionMyocardial Reperfusion InjuryNitric OxideOxidative StressPhosphatidylinositol 3-KinaseAcetylglucosamineAMP-Activated Protein KinasesArginaseBeclin-1MTOR protein, humanNitric OxidePhosphatidylinositol 3-KinasePRKAA1 protein, humanProto-Oncogene Proteins c-aktReactive Oxygen Speciesrho-Associated KinasesTOR Serine-Threonine KinasesAutophagyDiabetesHeartOxidative stressROCK

Identifiers

PMID30729392
OpenAlexW2913944640

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.