Evidence map›Paper›PMID 30073629›Full record

ArticleJournal of cell communication and signaling2019

Targeting necroptotic cell death pathway by high-intensity interval training (HIIT) decreases development of post-ischemic adverse remodelling after myocardial ischemia / reperfusion injury.

Alireza Ghardashi Afousi, Abbasali Gaeini, Kamran Rakhshan, Nasim Naderi, Amir Darbandi Azar, Nahid Aboutaleb

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cell communication and signaling, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

18 citing papers in PubMed, 37 citations in OpenAlex.

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  7. Pharmaceutical Therapies for Necroptosis in Myocardial Ischemia-Reperfusion Injury.Journal of cardiovascular development and disease · 2023
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  18. Guidelines for evaluating myocardial cell death.American journal of physiology. Heart and circulatory physiology · 2019
    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

6 authors at 2 institutions in 1 country.

Alireza Ghardashi AfousiDepartment of Exercise Physiology, Faculty of Physical Education and Exercise Sciences, University of Tehran, Tehran, IR, Iran.
Abbasali GaeiniDepartment of Exercise Physiology, Faculty of Physical Education and Exercise Sciences, University of Tehran, Tehran, IR, Iran.
Kamran RakhshanDepartment of Physiology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Nasim NaderiRajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran.
Amir Darbandi AzarRajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran.
Nahid AboutalebPhysiology Research Center and Department of Physiology, Iran University of Medical Sciences, Tehran, Iran. dr_nabo40@yahoo.com.ORCID http://orcid.org/0000-0002-7514-5939
Iran University of Medical Sciences · IRUniversity of Tehran · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regulated necrosis (necroptosis) plays a pivotal role in the extent of cardiomyocyte loss and the development of post-ischemic adverse remodelling and cardiac dysfunction following myocardial I/R injury. Although HIIT has been reported to give rise to cardioprotection against MI, but the detailed knowledge of its molecular targets for treatment of MI is still not available. The LAD of Male Wistar rats was occluded to induce MI for 30 min and reperfusion for eight weeks. We investigated the effect of long-term HIIT for eight weeks on lipid peroxidation, SOD activity and GSH content using ELISA assay. Cardiac function, fibrosis, and infarct size were assessed by echocardiography, Masson's trichrome and Evans Blue/TTC dual staining respectively. The expressions of gene markers of myocardial hypertrophy, fibrosis and key mediators of necroptosis were measured using RT-PCR and western blotting assay respectively. The results indicated that HIIT reduced lipid peroxidation, infarct size and improved endogenous antioxidant system and heart function. Significant decreases in mRNA levels of procollagen α1(I), α1(III), and fibronectin1were observed following HIIT. Moreover, that HIIT significantly decreased the expression of key mediators of necroptosis induced by MI (P < 0.05). There were no significant differences in β-MHC mRNA level in different groups. The findings of study suggest that HIIT might exert cardioprotective effects against post-ischemic adverse remodeling through targeting necroptosis process. Likewise, cardioprotective effects of HIIT in coping with myocardial I/R injury may be associated with RIP1-RIP3-MLKL axis. These findings establish a critical foundation for higher efficiency of exercise-based cardiac rehabilitation post-MI and future research.

Indexed as

High-intensity interval trainingMyocardial infarctionNecroptosisOxidative stressPost-ischemic adverse remodelling

Identifiers

PMID30073629
PMCPMC6498245
OpenAlexW2886935248

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.