ReviewNon-coding RNA research2025
The role of long non-coding RNAs in cardiovascular diseases: A comprehensive review.
Review in Non-coding RNA research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed.
- LncRNA H19 promotes vascular remodeling by inhibiting MFN2.Functional & integrative genomics · 2026Article
- Long non-coding RNAs as molecular hubs integrating inflammatory and osteogenic pathways in calcific aortic valve disease.Frontiers in cardiovascular medicine · 2026Review
- Epigenetic Modulation of Immunity: Mechanisms, Implications, and Emerging Therapeutic Horizons; a Step Toward Epigenetics to Precision.Sub-cellular biochemistry · 2026Review
- Non-coding RNA biomarkers in resistant hypertension: a scoping review.Frontiers in molecular biosciences · 2026Review
- Emerging roles of long non-coding RNAs in osteoarthritis: from molecular mechanisms to therapeutic opportunities.RNA biology · 2025Review
- Bioinformatics-based study on the regulatory network of lipid metabolism-related genes and mechanisms in coronary heart disease.Hereditas · 2025Article
- Unveiling the oncogenic functions of lncRNA PSMG3-AS1: a review of its biological roles in cancer.Discover oncology · 2025Review
- Cardioepigenetics in action: aerobic exercise-induced modulation of miRNAs, lncRNAs, and chromatin remodeling in cardiovascular disease.Frontiers in cardiovascular medicine · 2025Review
- Non-coding RNAs in heart failure: epigenetic regulatory mechanisms and therapeutic potential.Frontiers in genetics · 2025Review
- Cardiovascular diseases in the elderly: possibilities for modulating autophagy using non-coding RNAs.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiovascular diseases (CVDs) are the leading cause of morbidity and mortality worldwide, posing significant challenges to healthcare systems. Despite advances in medical interventions, the molecular mechanisms underlying CVDs are not yet fully understood. For decades, protein-coding genes have been the focus of CVD research. However, recent advances in genomics have highlighted the importance of long non-coding RNAs (lncRNAs) in cardiovascular health and disease. Changes in lncRNA expression specific to tissues may result from various internal or external factors, leading to tissue damage, organ dysfunction, and disease. In this review, we provide a comprehensive discussion of the regulatory mechanisms underlying lncRNAs and their roles in the pathogenesis and progression of CVDs, such as coronary heart disease, atherosclerosis, heart failure, arrhythmias, cardiomyopathies, and diabetic cardiomyopathy, to explore their potential as therapeutic targets and diagnostic biomarkers.
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Identifiers
What 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.