ReviewCurrent heart failure reports2017
From Inflammation to Fibrosis-Molecular and Cellular Mechanisms of Myocardial Tissue Remodelling and Perspectives on Differential Treatment Opportunities.
Review in Current heart failure reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 173 papers, 2 of them syntheses that pooled it.
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
173 citing papers in PubMed, 2 syntheses or guidelines pooled it, 304 citations in OpenAlex.
- A genomic meta-analysis of clinical variables and their association with intrinsic molecular subsets in systemic sclerosis.Rheumatology (Oxford, England) · 2022Pooled it
- Brazilian Society of Cardiology Guideline on Myocarditis - 2022.Arquivos brasileiros de cardiologia · 2022Guideline
- The Role of the Extracellular Volume of the Infarction Zone and the Remote Myocardium in Predicting Systolic Dysfunction After the First Myocardial Infarction.Diagnostics (Basel, Switzerland) · 2026Article
- Article
- Slick K+ channels contribute to cardiac remodeling, fibrosis, and dysfunction in postinfarction hearts.JCI insight · 2026Article
- Myocardial fibrosis and viability: the role of imaging and biomarkers in patients with chronic total occlusion on coronary angiography.Biochemia medica · 2026Review
- IGFBP7 and Heart Failure: From Senescence Biomarker to Therapeutic Target.Current heart failure reports · 2026Review
- Targeting C/EBPβ to Suppress Myocardial Fibrosis in Hypertensive Heart Disease: Role of the ACE2/Ang-(1-7) Pathway.Journal of cellular and molecular medicine · 2026Article
- Myocardial Expression of PD-L1 as a Marker of Poor Prognosis in Immune Checkpoint Inhibitor-Associated Myocarditis.JACC. CardioOncology · 2026Article
- Macrophages of the heart: Homeostasis and disease.Biomedical journal · 2026Review
- Electrocardiographic predictors of major adverse cardiovascular events in immune checkpoint inhibitor-associated myocarditis.Cardio-oncology (London, England) · 2026Article
- uPAR deficiency triggers TGFβ1-mediated fibrotic remodeling in a cardiac perivascular-like microenvironment.Stem cell research & therapy · 2026Article
- Doxorubicin-Induced Cardiac Remodeling: Mechanisms and Mitigation Strategies.Cardiovascular drugs and therapy · 2026Review
- Integrated risk stratification for ICI-associated myocarditis: a baseline hematological profile and a combined ECG and enzymatic signature at onset.Frontiers in immunology · 2026Article
- Potential Mechanisms of Sodium-Glucose Cotransporter 2 Inhibitors in Regulating Cardiac and Renal Fibrosis.Cardiorenal medicine · 2026Review
- Different forms of cardiomyocyte death in post-myocardial infarction ventricular remodeling: mechanisms and therapeutic strategies.Frontiers in cardiovascular medicine · 2026Review
- Protocatechuic acid and syringin improve cardiac damage and autonomic imbalance caused by dyslipidemia in mice.Frontiers in pharmacology · 2026Article
- Circulating microRNAs miR-21-5p, miR-23a-3p and miR-26a-5p reflect clinical and molecular features of aging.Scientific reports · 2025Article
- How Rapidly Does the FAPI PET Signal Reverse Following Therapy? Assessing the FAPI PET Signal in Hypertensive Cardiac Injury and Fibrosis in Mice.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2025Article
- Article
113 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
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose of reviewIn this review, we highlight the most important cellular and molecular mechanisms that contribute to cardiac inflammation and fibrosis. We also discuss the interplay between inflammation and fibrosis in various precursors of heart failure (HF) and how such mechanisms can contribute to myocardial tissue remodelling and development of HF. RECENT
findingsRecently, many research articles attempt to elucidate different aspects of the interplay between inflammation and fibrosis. Cardiac inflammation and fibrosis are major pathophysiological mechanisms operating in the failing heart, regardless of HF aetiology. Currently, novel therapeutic options are available or are being developed to treat HF and these are discussed in this review. A progressive disease needs an aggressive management; however, existing therapies against HF are insufficient. There is a dynamic interplay between inflammation and fibrosis in various precursors of HF such as myocardial infarction (MI), myocarditis and hypertension, and also in HF itself. There is an urgent need to identify novel therapeutic targets and develop advanced therapeutic strategies to combat the syndrome of HF. Understanding and describing the elements of the inflammatory and fibrotic pathways are essential, and specific drugs that target these pathways need to be evaluated.
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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.