ReviewCardiovascular drugs and therapy2026
DNA/RNA Methylation-Driven Coronary Microvascular Dysfunction: Emerging Pathogenic Mechanisms and Therapeutic Opportunities for Heart Failure in Diabetes.
Review in Cardiovascular drugs and therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- Beyond Epigenetic Memory: A Proposed Immune-redox Framework for Coronary Microvascular Dysfunction in Diabetes.Cardiovascular drugs and therapy · 2026Article
- PRMT2 Aggravates Pressure Overload-induced Cardiac Remodeling by Promoting Endothelial Phenotypic Transition via Snail1 Methylation.Cardiovascular drugs and therapy · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Coronary microvascular dysfunction (CMD) is an established pathological driver of heart failure, with endothelial cell (EC) dysfunction representing a central determinant of its development and progression. EC impairment disrupts normal coronary microvascular tone and perfusion, and promotes myocardial inflammation, fibrosis, and cardiomyocyte stress, as characteristic features of the diabetic heart. CMD is often clinically silent and undiagnosed, whilst conventional therapies targeting cardiometabolic risk factors are largely ineffective towards restoring microvascular integrity. Emerging evidence implicates epigenetic dysregulation, including DNA and RNA methylation, as a critical mechanism underlying maladaptive EC signalling. These key modifications encode microvascular memory, sustaining endothelial dysfunction even after risk factors are optimally controlled; DNA methylation stabilises pathogenic transcription whilst RNA methylation regulates transcript stability and translation to support continued disruption of EC homeostasis. Indeed, preclinical studies demonstrate that pharmacological DNA methylation inhibitors and RNA methylation modulators can restore healthy EC function, reflected by reduced inflammation and preserved microvascular integrity, positioning such epigenetic pathways as central determinants of CMD with clear mechanistic relevance and therapeutic potential. Selective methylation targeting therefore offers exciting translational promise to reprogram dysfunctional ECs in diabetic patients, reversing CMD and preventing development and progression of associated heart failure. This timely review summarises current knowledge of EC epigenetic regulation, focusing on methylation modifications, and explores how emerging mechanistic insights may be leveraged to advance therapeutic targeting of CMD in the diabetic heart as foundation for development of innovative clinical management strategies.
Indexed as
Identifiers
42432348What OpenQuestion holds
Registered trials
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.