ReviewCirculation research2025
Cardiac Fibrosis in the Multi-Omics Era: Implications for Heart Failure.
Review in Circulation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 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
67 citing papers in PubMed.
- Breaking the cycle of fibrosis: Ferroptosis as a therapeutic target (Review).International journal of molecular medicine · 2026Review
- Gfpt2 modulates fibroblast activation by glutathione metabolism.Journal of molecular and cellular cardiology · 2026Article
- Cardiac proteomic and phosphoproteomic profiling defines clinically relevant molecular subgroups in human heart failure.Nature cardiovascular research · 2026Article
- Mitochondrial heterogeneity across cardiac cell types in heart failure with preserved ejection fraction.Redox biology · 2026Review
- The Wound-Heart Axis: Can Chronic Wounds Contribute to Cardiac Dysfunction?International journal of molecular sciences · 2026Review
- AI-Powered Detection of Left Ventricular Myocardial Scar from Dual-Sequence CT: Global and Segmental Prediction Validated by CMR.Journal of imaging informatics in medicine · 2026Article
- Increased NETosis in Patients With Heart Failure Is Associated With Macrophage Activation Towards a Proinflammatory Phenotype.Journal of cellular and molecular medicine · 2026Article
- Heart Failure with Reduced versus Preserved Ejection Fraction: Molecular Mechanisms, Immunologic Pathways, Current Therapies, and Future Directions.Archives of internal medicine research · 2026Article
- SerpinA3 is an Endogenous TGF-β Receptor Antagonist that Attenuates Cardiac Fibroblast Activation and Fibrotic Remodeling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Multiple triggering mechanisms of myocardial fibrosis: Comparison and integration in different disease contexts.iScience · 2026Review
- Dual-Metal Regulation of Cardiac Remodeling: Targeting the LOXL2-Ferroptosis Axis in Metal-Induced Cardiac Dysfunction.Cardiovascular toxicology · 2026Review
- Review
- Heart Failure with Reduced and Mildly Reduced Ejection Fraction: A Network Interpretive Framework of Mechanisms, Phenotypes, and Therapeutic Response.International journal of molecular sciences · 2026Review
- Shared mechanisms of organ fibrosis.JCI insight · 2026Review
- Stanniocalcin-1 Attenuates Cardiac Fibrosis Post Ischemia-Reperfusion Injury by Targeting the DOCKER Domain of Dedicator of Cytokinesis 1.Journal of the American Heart Association · 2026Article
- Myocardial Immune Niches in Homeostasis and Inflammation.Immunological reviews · 2026Review
- Effects of Low-Intensity Aaerobic Training on Cardiac Dysfunction and Myocardial Fibrosis Induced by Doxorubicin in Wistar Rats.Cardiovascular toxicology · 2026Article
- Review
- Integrative Bioinformatics and Experimental Validation Identify LOX as a Glycolysis-Related Biomarker in Myocardial Ischemia-Reperfusion Injury.Cardiovascular toxicology · 2026Article
- Mitochondrial UQCRC2 as a Redox-Regulatory Node in Metabolic and Cardiometabolic Diseases.Antioxidants (Basel, Switzerland) · 2026Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Cardiac fibrosis, a hallmark of heart failure and various cardiomyopathies, represents a complex pathological process that has long challenged therapeutic intervention. High-throughput omics technologies have begun revolutionizing our understanding of the molecular mechanisms driving cardiac fibrosis and are providing unprecedented insights into its heterogeneity and progression. This review provides a comprehensive analysis of how techniques-encompassing genomics, epigenomics, transcriptomics, proteomics, and metabolomics-are providing insight into our understanding of cardiac fibrosis. Genomic studies have identified novel genetic variants and regulatory networks associated with fibrosis susceptibility and progression, and single-cell transcriptomics has unveiled distinct cardiac fibroblast subpopulations with unique molecular signatures. Epigenomic profiling has revealed dynamic chromatin modifications controlling fibroblast activation states, and proteomic analyses have identified novel biomarkers and potential therapeutic targets. Metabolomic studies have uncovered important alterations in cardiac energetics and substrate utilization during fibrotic remodeling. The integration of these multi-omic data sets has led to the identification of previously unrecognized pathogenic mechanisms and potential therapeutic targets, including cell-type-specific interventions and metabolic modulators. We discuss how these advances are driving the development of precision medicine approaches for cardiac fibrosis while highlighting current challenges and future directions in translating multi-omic insights into effective therapeutic strategies. This review provides a systems-level perspective on cardiac fibrosis that may inform the development of more effective, personalized therapeutic approaches for heart failure and related cardiovascular diseases.
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Registered trials
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