ReviewCellular signalling2021
Adding insult to injury - Inflammation at the heart of cardiac fibrosis.
Review in Cellular signalling, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 60 citations in OpenAlex.
- Beyond the Heart-Lung Axis: A Review of the Crosstalk Between the Hemodynamic, Neurohormonal, and Immune Systems in Pulmonary Hypertension.Comprehensive physiology · 2026Review
- Molecular imaging of immune and fibrosis targets to guide therapy for repair after myocardial infarction.Nature reviews. Cardiology · 2026Review
- CC Chemokines in Myocardial Fibrosis: Regulatory Networks of CCL17 and Emerging Therapeutic Implications.International journal of molecular sciences · 2026Review
- Disruption of the Fibroinflammatory Loop: A Therapeutic Strategy for Cardiac Fibrosis in Non-Ischemic Cardiomyopathy.Reviews in cardiovascular medicine · 2026Article
- IFN-γ and TNF-α Impair Lung Development by Upregulating SMAD7 to Inhibit TGF-β Signaling Pathway and ECM Dysregulation.Inflammation · 2026Article
- Retinoic acid promotes expression of inflammatory factors in proliferative adult human heart cells.American journal of physiology. Cell physiology · 2026Article
- Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026Review
- Engineered T cell therapy for the treatment of cardiac fibrosis during chronic phase of myocarditis.Theranostics · 2026Article
- c-Myc: an emerging participant in heart failure.Frontiers in cardiovascular medicine · 2026Review
- Inhibition of HuR/ELAVL-1 attenuates fibrotic progression in Mdx mice with dilated cardiomyopathy.Cellular and molecular life sciences : CMLS · 2025Article
- Activation/inactivation of Tregs mediated by Kv1.3 potassium channels synergistically with exosome secretion to regulate myocardial fibrosis.Scientific reports · 2025Article
- Sex differences in a murine model of infective endocarditis.Basic research in cardiology · 2025Article
- Toll-like Receptors 1, 3 and 7 Activate Distinct Genetic Features of NF-κB Signaling and γ-Protocadherin Expression in Human Cardiac Fibroblasts.Inflammation · 2025Article
- Cardiomyocyte YAP represses myocardial inflammation and fibrosis and restrains MEF2-regulated gene expression.American journal of physiology. Heart and circulatory physiology · 2025Article
- Association Between Dietary Patterns and Lifestyle Habits with Vascular Inflammatory Responses in Individuals with Hypertension Living in PMDiseases (Basel, Switzerland) · 2025Article
- Cardiovascular, Kidney, Liver, and Metabolic Interactions in Heart Failure: Breaking Down Silos.Circulation research · 2025Review
- Immune Regulation in Atrial Cardiomyopathy.Reviews in cardiovascular medicine · 2025Review
- Morphometric and Molecular Interplay in Hypertension-Induced Cardiac Remodeling with an Emphasis on the Potential Therapeutic Implications.International journal of molecular sciences · 2025Review
- Hypertrophic heart failure promotes gut dysbiosis and gut leakage in interleukin 10-deficient mice.American journal of physiology. Heart and circulatory physiology · 2025Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The fibrotic response has evolutionary worked in tandem with the inflammatory response to facilitate healing following injury or tissue destruction as a result of pathogen clearance. However, excessive inflammation and fibrosis are key pathological drivers of organ tissue damage. Moreover, fibrosis can occur in several conditions associated with chronic inflammation that are not directly caused by overt tissue injury or infection. In the heart, in particular, fibrotic adverse cardiac remodeling is a key pathological driver of cardiac dysfunction in heart failure. Cardiac fibroblast activation and immune cell activation are two mechanistic domains necessary for fibrotic remodeling in the heart, and, independently, their contributions to cardiac fibrosis and cardiac inflammation have been studied and reviewed thoroughly. The interdependence of these two processes, and how their cellular components modulate each other's actions in response to different cardiac insults, is only recently emerging. Here, we review recent literature in cardiac fibrosis and inflammation and discuss the mechanisms involved in the fibrosis-inflammation axis in the context of specific cardiac stresses, such as myocardial ischemia, and in nonischemic heart conditions. We discuss how the search for anti-inflammatory and anti-fibrotic therapies, so far unsuccessful to date, needs to be based on our understanding of the interdependence of immune cell and fibroblast activities. We highlight that in addition to the extensively reviewed role of immune cells modulating fibroblast function, cardiac fibroblasts are central participants in inflammation that may acquire immune like cell functions. Lastly, we review the gut-heart axis as an example of a novel perspective that may contribute to our understanding of how immune and fibrotic modulation may be indirectly modulated as a potential area for therapeutic research.
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.