Article3 Biotech2024
Ischemic preconditioning modulates the DNA methylation process of the rat heart to provide tolerance to withstand ischemia reperfusion injury and its associated mitochondrial dysfunction.
Article in 3 Biotech, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Phase-dependent iron dysmetabolism in myocardial ischemia-reperfusion injury: From mechanisms to therapies.American heart journal plus : cardiology research and practice · 2025Review
- Ischaemic preconditioning regulates cardiac transcriptome via DNA methylation conferring cardio-protection from ischaemic reperfusion injury.European heart journal open · 2025Article
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2 authors at 1 institution in 1 country.
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Abstract
DNA methylation plays a crucial role in the pathogenesis of myocardial ischemia reperfusion injury(I/R) and the I/R injury can be combated effectively by ischemia preconditioning (IPC), but the role is DNA methylation in this process is unknown. In this study, we uncovered the role of ischemic preconditioning (IPC)- mediated cardioprotection of rat myocardium by using a Langendorff rat heart model with 30 min of ischemia followed by 60 min of reperfusion. Heart conditioned with short cycles of ischemia and reperfusion (IPC procedure) prior to I/R protocol significantly reduced the I/R-induced global DNA hypermethylation level by 32% and the DNMT activity by 33% while rendering cardioprotection. Blocking the PI3K pathway via wortmannin not only negates the cardio-protection by IPC, but also increases the methylation of DNA by 75%. Besides, the correlation analysis showed a negative relationship between PI3K gene expression and the global DNA methylation level ( Supplementary Information: The online version contains supplementary material available at 10.1007/s13205-024-03965-0.
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