ReviewFrontiers in physiology2020
Leukocyte-Dependent Regulation of Cardiac Fibrosis.
Review in Frontiers in physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 43 citations in OpenAlex.
- Myocardial fibrosis and glycolysis: a bibliometric study and visualization analysis (2000-2024).Journal of translational medicine · 2026Review
- Article
- Multifaceted roles of neutrophils in cardiac disease.Journal of leukocyte biology · 2025Review
- Complex regulation of cardiac fibrosis: insights from immune cells and signaling pathways.Journal of translational medicine · 2025Review
- Immunological Regulation of Fibrosis During Heart Failure: It Takes Two to Tango.Biomolecules · 2025Review
- Article
- The Current State of Extracellular Matrix Therapy for Ischemic Heart Disease.Medical sciences (Basel, Switzerland) · 2024Review
- Meta-analysis of Pulsed Field Ablation Versus Thermal Ablation for Pulmonary Vein Isolation in AF: A Broad Overview Focusing on Efficacy, Safety and Outcomes.Arrhythmia & electrophysiology review · 2024Review
- Cardiac fibrogenesis: an immuno-metabolic perspective.Frontiers in physiology · 2024Review
- Extracellular Matrix Protein-1 as a Mediator of Inflammation-Induced Fibrosis After Myocardial Infarction.JACC. Basic to translational science · 2023Article
- Myeloid cell-specific deletion of epidermal growth factor receptor aggravates acute cardiac injury.Clinical science (London, England : 1979) · 2023Article
- Visualization of fibroblast activation usingJournal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2023Article
- Beyond cardiomyocytes: Cellular diversity in the heart's response to exercise.Journal of sport and health science · 2023Review
- βTrends in molecular medicine · 2023Article
- Bioinformatics analysis of the genes associated with co-occurrence of heart failure and lung cancer.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- The Pathogenic Role of Oxidative Stress, Cytokine Expression, and Impaired Hematological Indices in Diabetic Cardiovascular Diseases.Inflammation · 2023Article
- Progress on role of ion channels of cardiac fibroblasts in fibrosis.Frontiers in physiology · 2023Review
- Subtyping based on immune cell fractions reveal heterogeneity of cardiac fibrosis in end-stage heart failure.Frontiers in immunology · 2023Article
- Interferon-β decreases LPS-induced neutrophil recruitment to cardiac fibroblasts.Frontiers in cell and developmental biology · 2023Article
- The cardiosplenic axis: the prognostic role of the spleen in heart failure.Heart failure reviews · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cardiac fibrosis begins as an intrinsic response to injury or ageing that functions to preserve the tissue from further damage. Fibrosis results from activated cardiac myofibroblasts, which secrete extracellular matrix (ECM) proteins in an effort to replace damaged tissue; however, excessive ECM deposition leads to pathological fibrotic remodeling. At this extent, fibrosis gravely disturbs myocardial compliance, and ultimately leads to adverse outcomes like heart failure with heightened mortality. As such, understanding the complexity behind fibrotic remodeling has been a focal point of cardiac research in recent years. Resident cardiac fibroblasts and activated myofibroblasts have been proven integral to the fibrotic response; however, several findings point to additional cell types that may contribute to the development of pathological fibrosis. For one, leukocytes expand in number after injury and exhibit high plasticity, thus their distinct role(s) in cardiac fibrosis is an ongoing and controversial field of study. This review summarizes current findings, focusing on both direct and indirect leukocyte-mediated mechanisms of fibrosis, which may provide novel targeted strategies against fibrotic remodeling.
Indexed as
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.