Evidence map›Paper›PMID 41132408›Full record

ArticleEuropean heart journal open2025

Ischaemic preconditioning regulates cardiac transcriptome via DNA methylation conferring cardio-protection from ischaemic reperfusion injury.

Abdul Waheed Khan, Shafaat Hussain, Ahmed Elmahdy, Yalda Kakaei, Aaron Shekka Espinosa, Abhishek Jha, Elmir Omerovic, Misbah Aziz, Scott Maxwell, Karin A M Jandeleit-Dahm and 1 more

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Article in European heart journal open, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. 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

11 authors.

Abdul Waheed KhanDepartment of Diabetes, School of Translational Medicine, Monash University, Level 5, 99 Commercial Road, Melbourne 3004, Australia.ORCID https://orcid.org/0000-0001-6626-6897
Shafaat HussainDepartment of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University, PO Box 100, 405 30 Gothenburg, Sweden.
Ahmed ElmahdyDepartment of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University, PO Box 100, 405 30 Gothenburg, Sweden.
Yalda KakaeiDepartment of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University, PO Box 100, 405 30 Gothenburg, Sweden.
Aaron Shekka EspinosaDepartment of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University, PO Box 100, 405 30 Gothenburg, Sweden.
Abhishek JhaDepartment of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University, PO Box 100, 405 30 Gothenburg, Sweden.
Elmir OmerovicDepartment of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University, PO Box 100, 405 30 Gothenburg, Sweden.ORCID https://orcid.org/0000-0002-3875-8621
Misbah AzizDepartment of Diabetes, School of Translational Medicine, Monash University, Level 5, 99 Commercial Road, Melbourne 3004, Australia.
Scott MaxwellDepartment of Diabetes, School of Translational Medicine, Monash University, Level 5, 99 Commercial Road, Melbourne 3004, Australia.
Karin A M Jandeleit-DahmDepartment of Diabetes, School of Translational Medicine, Monash University, Level 5, 99 Commercial Road, Melbourne 3004, Australia.
Bjorn RedforsDepartment of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg University, PO Box 100, 405 30 Gothenburg, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aims: Myocardial ischaemic preconditioning (IPC) increases myocardial ability to withstand ischaemic injury. Myocardial stunning is a reversible dysfunction, while necrosis results in irreversible cell death. The link between IPC, stunning, and necrosis remains unclear. This study aimed to utilize a novel 13.5-min ischaemia-reperfusion (I/R) rat model, distinct from conventional I/R models, to identify transcriptomic changes associated with IPC and investigate the role of DNA methylation in regulating these changes, particularly in relation to myocardial stunning and necrosis. Methods and results: A novel rat model of cardiac I/R injury was used, with IPC induced by two 5-min ischaemia-reperfusion cycles followed by 13.5-min of ischaemia, and a control group undergoing 13.5-min of ischaemia without IPC. Myocardial samples were collected at early (T1) and 4-h (T2) post-reperfusion, representing stunned myocardium in the IPC group and necrosis in the control group. RNA sequencing, DNA methyltransferase (DNMT) activity assay, Chromatin immunoprecipitation (ChIP), and DNA methylation analyses were performed. IPC reprogrammed the cardiac transcriptome, with 53 genes differentially expressed at T1 and 166 at T2, including key regulators of inflammation (Nfkbia), DNA repair (Gadd45b, Parp14), and stress responses (Cebpd, Jun). IPC reduced global DNMT activity, promoting hypomethylation of protective genes like Conclusion: IPC re-programmes the cardiac transcriptome through dynamic DNA methylation, enhancing myocardial resilience while increasing stunning as an adaptive mechanism to limit necrosis.

Indexed as

Cardiac transcriptomicsDNA methylationIschaemia-reperfusion injuryMyocardial infarctionMyocardial ischaemic preconditioning: Myocardial stunning

Identifiers

PMID41132408
PMCPMC12541389

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