ArticleThe American journal of pathology2002
Complement and dilated cardiomyopathy: a role of sublytic terminal complement complex-induced tumor necrosis factor-alpha synthesis in cardiac myocytes.
Article in The American journal of pathology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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.
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Who cites it
27 citing papers in PubMed, 66 citations in OpenAlex.
- An integrated cell atlas of 2.4 million cardiac cells across 209 individuals in health and disease.Nature cardiovascular research · 2026Article
- Large-Scale Proteomic Profiling of Incident Heart Failure and Its Subtypes in Older Adults.Circulation. Genomic and precision medicine · 2026Article
- Functional Roles of the Complement Immune System in Cardiac Inflammation and Hypertrophy.International journal of molecular sciences · 2025Review
- Selective C-reactive protein apheresis in acute myocardial infarction: rationale and design of a prospective international randomized controlled trial.Coronary artery disease · 2025Article
- Complement-mediated and direct activation of human neutrophils induced byFrontiers in immunology · 2025Article
- The Role of BAG3 Protein Interactions in Cardiomyopathies.International journal of molecular sciences · 2024Article
- Article
- Proteomic Profiling of Dilated Cardiomyopathy Plasma Samples ─ Searching for Biomarkers with Potential to Predict the Outcome of Therapy.Journal of proteome research · 2024Article
- Acylation-stimulating protein and heart failure progression in arrhythmogenic right ventricular cardiomyopathy.ESC heart failure · 2023Article
- Identification and analysis of differential miRNA-mRNA interactions in coronary heart disease: an experimental screening approach.Frontiers in cardiovascular medicine · 2023Article
- Cardiovascular changes in the NZB/W F1 mouse model of lupus nephritis.Frontiers in cardiovascular medicine · 2023Article
- Mechanisms of COVID-19 pathogenesis in diabetes.American journal of physiology. Heart and circulatory physiology · 2022Review
- PhIP-Seq Reveals Autoantibodies for Ubiquitously Expressed Antigens in Viral Myocarditis.Biology · 2022Article
- Immunomodulatory Treatment Strategies Targeting B Cells for Heart Failure.Frontiers in pharmacology · 2022Review
- The role of B cells in heart failure and implications for future immunomodulatory treatment strategies.ESC heart failure · 2020Review
- Mediastinal Lymphadenopathy, Class-Switched Auto-Antibodies and Myocardial Immune-Complexes During Heart Failure in Rodents and Humans.Frontiers in cell and developmental biology · 2020Article
- Increased circulating IgG levels, myocardial immune cells and IgG deposits support a role for an immune response in pre- and end-stage heart failure.Journal of cellular and molecular medicine · 2019Article
- Article
- Complement anaphylatoxin C3a as a novel independent prognostic marker in heart failure.Clinical research in cardiology : official journal of the German Cardiac Society · 2012Article
- Membrane attack by complement: the assembly and biology of terminal complement complexes.Immunologic research · 2011Review
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dilated cardiomyopathy is a syndrome characterized by cardiac enlargement and impaired systolic function of the heart. Tumor necrosis factor (TNF)-alpha, a pleiotropic cytokine, seems to play a central role in the progression of dilated cardiomyopathy. Recent data suggest that ongoing inflammation in the myocardium may, in many cases, contribute to the development of disease. Chronic generation of autoantibodies to myocardial antigens or, in some cases, viral infection are pathobiologically involved. Although both antibodies and some viruses activate the complement system, the role of innate immunity in dilated cardiomyopathy has as yet not been investigated systematically. In this study we demonstrate by analysis of myocardial biopsies from 28 patients that C5b-9, the terminal membrane attack complex of complement, accumulates in human myocardium in dilated cardiomyopathy. C5b-9 significantly correlates with immunoglobulin deposition and myocardial expression of TNF-alpha. In vitro, C5b-9 attack on cardiac myocytes induces nuclear factor (NF)-kappaB activation as well as transcription, synthesis, and secretion of TNF-alpha. We conclude that chronic immunoglobulin-mediated complement activation in the myocardium may contribute in part to the progression of dilated cardiomyopathy via C5b-9-induced TNF-alpha expression in cardiac myocytes.
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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.