ReviewInternational journal of molecular sciences2020
Innate Immunity Effector Cells as Inflammatory Drivers of Cardiac Fibrosis.
Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
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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.
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Who cites it
50 citing papers in PubMed, 65 citations in OpenAlex.
- Multiple triggering mechanisms of myocardial fibrosis: Comparison and integration in different disease contexts.iScience · 2026Review
- Myeloid Cdc42 deficiency-mediated macrophage pyroptosis exacerbates diabetic cardiomyopathy in type 1 diabetes mellitus.Cardiovascular diabetology · 2026Article
- Disruption of the Fibroinflammatory Loop: A Therapeutic Strategy for Cardiac Fibrosis in Non-Ischemic Cardiomyopathy.Reviews in cardiovascular medicine · 2026Article
- Pro- and Anti-Inflammatory Cytokines' Implication in Right Heart Disease, Arrhythmogenesis, and Atrial Fibrillation.Biomolecules · 2026Review
- Immune response in dogs with myxomatous mitral valve disease: insights into monocyte and lymphocyte subtypes and natural killer cells.Journal of veterinary internal medicine · 2026Article
- Immune Cell-Mediated Inflammation in Heart Failure: Subset Heterogeneity and Targeted Therapy.International journal of general medicine · 2026Review
- Integrating mechanical cues inFrontiers in immunology · 2026Review
- SASP-mediated cellular senescence following myocardial infarction: from spatiotemporal immune regulation to therapeutic strategies.Frontiers in immunology · 2026Review
- Neurocardiac consequences of traumatic brain injury: integrating neuroimmune, autonomic, and cerebrovascular mechanisms.Frontiers in immunology · 2026Review
- Activation/inactivation of Tregs mediated by Kv1.3 potassium channels synergistically with exosome secretion to regulate myocardial fibrosis.Scientific reports · 2025Article
- Oxidative Stress and NLRP3 Inflammasome as Markers of Cardiac Injury Following Cardiopulmonary Bypass: Potential Implications for Patients with Preoperative Heart Failure with Reduced Ejection Fraction.Antioxidants (Basel, Switzerland) · 2025Article
- Identification and Verification of Potential Markers Related to Myocardial Fibrosis by Bioinformatics Analysis.Biochemical genetics · 2025Review
- Comparison of six surrogate insulin resistance indices for predicting the accumulation of pericardial fat on noncontrast computed tomography.Quantitative imaging in medicine and surgery · 2025Article
- A critical role for IL-21/IL-21 receptor signaling in isoproterenol-induced cardiac remodeling.Scientific reports · 2025Article
- Immune Regulation in Atrial Cardiomyopathy.Reviews in cardiovascular medicine · 2025Review
- The functions of immune system-derived miRNAs in cardiovascular diseases.Non-coding RNA research · 2025Review
- Decoding the regulatory roles of circular RNAs in cardiac fibrosis.Non-coding RNA research · 2025Review
- Transcriptional meta-analysis and immune cell profiles reveal altered neutrophil dynamics in chronic atrial fibrillation.Royal Society open science · 2025Article
- The immunology of diabetic cardiomyopathy.Frontiers in endocrinology · 2025Review
- NETs drive myocardial fibrosis in hypertension via an NF-κB/ferroptosis axis.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Despite relevant advances made in therapies for cardiovascular diseases (CVDs), they still represent the first cause of death worldwide. Cardiac fibrosis and excessive extracellular matrix (ECM) remodeling are common end-organ features in diseased hearts, leading to tissue stiffness, impaired myocardial functional, and progression to heart failure. Although fibrosis has been largely recognized to accompany and complicate various CVDs, events and mechanisms driving and governing fibrosis are still not entirely elucidated, and clinical interventions targeting cardiac fibrosis are not yet available. Immune cell types, both from innate and adaptive immunity, are involved not just in the classical response to pathogens, but they take an active part in "sterile" inflammation, in response to ischemia and other forms of injury. In this context, different cell types infiltrate the injured heart and release distinct pro-inflammatory cytokines that initiate the fibrotic response by triggering myofibroblast activation. The complex interplay between immune cells, fibroblasts, and other non-immune/host-derived cells is now considered as the major driving force of cardiac fibrosis. Here, we review and discuss the contribution of inflammatory cells of innate immunity, including neutrophils, macrophages, natural killer cells, eosinophils and mast cells, in modulating the myocardial microenvironment, by orchestrating the fibrogenic process in response to tissue injury. A better understanding of the time frame, sequences of events during immune cells infiltration, and their action in the injured inflammatory heart environment, may provide a rationale to design new and more efficacious therapeutic interventions to reduce cardiac fibrosis.
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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.