ReviewHeart failure reviews2014
Fibrosis and heart failure.
Review in Heart failure reviews, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 181 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
181 citing papers in PubMed.
- Effect of Colchicine in reducing MMP-9, NOX2, and TGF- β1 after myocardial infarction.BMC cardiovascular disorders · 2023Trial
- Cardiac magnetic resonance imaging reveals myocardial fibrosis and systolic dysfunction in mitochondrial trifunctional protein-deficient mice.Disease models & mechanisms · 2026Article
- Ro5-4864, a ligand of the mitochondrial translocator protein, protects against heart failure in mice via regulation of the p62-Keap1-Nrf2 axis.The Journal of physiology · 2026Article
- Involvement of Fibulin-5 in endothelial to mesenchymal transition leading to cardiac fibrosis during metabolic syndrome.Journal of translational medicine · 2026Article
- Lactylation landscape of mitochondrial proteins in myocardial infarction.Redox biology · 2026Article
- Absence of GDF15 Aggravates Pressure Overload-Induced Cardiac Remodelling in Mice Hallmarked by Perivascular Fibrosis and Signs of Endothelial-to-Mesenchymal Transition.International journal of molecular sciences · 2026Article
- Neutrophil Gelatinase-Associated Lipocalin Drives Cardiac Remodeling in Rats With Chronic Kidney Disease.Hypertension (Dallas, Tex. : 1979) · 2026Article
- The role of mitochondrial dysfunction, oxidative stress, and gender in cardiac fibrosis and vascular remodeling in an induced aged rat model with possible mitigation by eugenol nano-emulsion.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Ganoderic Acid A Attenuates Pathological Cardiac Hypertrophy by Attenuating Inflammatory Responses.Current issues in molecular biology · 2026Article
- VCAM-1/Ezrin axis antagonizes myocardial damage in ischemia-reperfusion injury.Cell death and differentiation · 2026Article
- Lactylation landscape of mitochondrial proteins in myocardial infarction.bioRxiv : the preprint server for biology · 2026Article
- Association of Visual Heart Score with Gross Lung Pathology and Histology of Hepatic and Cardiopulmonary Tissues in Cattle at Harvest.Animals : an open access journal from MDPI · 2026Article
- Stem Cells and Their Derivatives in Cardiac Fibrosis Therapy: Challenges and Perspectives.Cells · 2026Review
- Empagliflozin Attenuates Cardiac Fibrosis by Suppressing Fibroblast-Mediated C-C Motif Chemokine Ligand 2 Expression.Journal of the American Heart Association · 2026Article
- Left Ventricular Ejection Fraction and Incident Cardiac Conduction Dysfunction: Exploring the Mediating Effects of Electrophysiological Parameters.Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc · 2026Article
- Integrated microarray-based and single-cell transcriptomic analyses reveal cell adhesion-related fibrotic remodeling signatures in heart failure.Frontiers in molecular biosciences · 2026Article
- Fructose and salt induce sex- and ovary dependent cardiac hypertrophy in Dahl salt-sensitive rats.Frontiers in cardiovascular medicine · 2026Article
- Molecular Mechanisms and Therapeutic Strategies Targeting Cardiac Lymphangiogenesis in Heart Failure.Cardiovascular toxicology · 2025Review
- The role of nitric oxide and connexin 43 in the cardioprotective effects of apigenin against doxorubicin-induced cardiotoxicity in male rats.Molecular biology reports · 2025Article
- Glycolysis to lactylation: Unraveling the metabolic and epigenetic landscape in tissue fibrosis (Review).Molecular medicine reports · 2025Review
121 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
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The extracellular matrix (ECM) is a living network of proteins that maintains the structural integrity of the myocardium and allows the transmission of electrical and mechanical forces between the myocytes for systole and diastole. During ventricular remodeling, as a result of iterations in the hemodynamic workload, collagen, the main component of the ECM, increases and occupies the areas between the myocytes and the vessels. The resultant fibrosis (reparative fibrosis) is initially a compensatory mechanism and may progress adversely influencing tissue stiffness and ventricular function. Replacement fibrosis appears at sites of previous cardiomyocyte necrosis to preserve the structural integrity of the myocardium, but with the subsequent formation of scar tissue and widespread distribution, it has adverse functional consequences. Continued accumulation of collagen impairs diastolic function and compromises systolic mechanics. Nevertheless, the development of fibrosis is a dynamic process wherein myofibroblasts, the principal cellular elements of fibrosis, are not only metabolically active and capable of the production and upregulation of cytokines but also have contractile properties. During the process of reverse remodeling with left ventricular assist device unloading, cellular, structural, and functional improvements are observed in terminal heart failure patients. With the advent of anti-fibrotic pharmacologic therapies, cellular therapy, and ventricular support devices, fibrosis has become an important therapeutic target in heart failure patients. Herein, we review the current concepts of fibrosis as a main component of ventricular remodeling in heart failure patients. Our aim is to integrate the histopathologic process of fibrosis with the neurohormonal, cytochemical, and molecular changes that lead to ventricular remodeling and its physiologic consequences in patients. The concept of fibrosis as living scar allows us to envision targeting this scar as a means of improving ventricular function in heart failure patients.
Indexed as
Identifiers
23124941What 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.