ArticleStem cells (Dayton, Ohio)2014
Complement component 3 is necessary to preserve myocardium and myocardial function in chronic myocardial infarction.
Article in Stem cells (Dayton, Ohio), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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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
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Transcriptomic data meta-analysis reveals common and injury model specific gene expression changes in the regenerating zebrafish heart.Scientific reports · 2023Pooled it
- Complement C5 inhibition with eculizumab or ravulizumab is associated with increased cardiovascular and thromboembolic risk after ST-elevation myocardial infarction: a propensity-matched global retrospective cohort study.BMC cardiovascular disorders · 2026Observational
- Complosome Activation after Myocardial Infarction in a Murine Model of Permanent LAD Ligation.Stem cell reviews and reports · 2026Article
- Proteomic results indicate inhibition of complement cascades is one of the mechanisms underlying the protective effects of Tongxinluo against myocardial infarction.Frontiers in pharmacology · 2026Article
- Transcriptomic dynamics of cardiac remodeling after myocardial infarction.Scientific reports · 2025Article
- Functional Roles of the Complement Immune System in Cardiac Inflammation and Hypertrophy.International journal of molecular sciences · 2025Review
- Human myocardial-derived highly proliferative cells improve cardiac remodeling after myocardial infarction in mice.The Journal of pharmacology and experimental therapeutics · 2025Article
- Reward system activation improves recovery from acute myocardial infarction.Nature cardiovascular research · 2024Article
- Linking the brain to recovery after myocardial infarction.Nature cardiovascular research · 2024Article
- The Complement System in the Central Nervous System: From Neurodevelopment to Neurodegeneration.Biomolecules · 2022Review
- Intracellular Complement Component 3 Attenuated Ischemia-Reperfusion Injury in the Isolated Buffer-Perfused Mouse Heart and Is Associated With Improved Metabolic Homeostasis.Frontiers in immunology · 2022Article
- Cardiac regenerative capacity: an evolutionary afterthought?Cellular and molecular life sciences : CMLS · 2021Review
- Immunomodulation for optimal cardiac regeneration: insights from comparative analyses.NPJ Regenerative medicine · 2021Review
- Serum complement C3 and islet β-cell function in patients with type 2 diabetes: A 4.6-year prospective follow-up study.Endocrine · 2020Article
- Transcriptome analysis defines myocardium gene signatures in children with ToF and ASD and reveals disease-specific molecular reprogramming in response to surgery with cardiopulmonary bypass.Journal of translational medicine · 2020Article
- Analysis of mesenchymal stem cell proteomesTheranostics · 2020Article
- Glycoproteomic Profiling Provides Candidate Myocardial Infarction Predictors of Later Progression to Heart Failure.ACS omega · 2019Article
- Unravelling the effects of mechanical physiological conditioning on cardiac adipose tissue-derived progenitor cells in vitro and in silico.Scientific reports · 2018Article
- Bioactive Sphingolipids, Complement Cascade, and Free Hemoglobin Levels in Stable Coronary Artery Disease and Acute Myocardial Infarction.Mediators of inflammation · 2018Article
- The Lectin Pathway of Complement in Myocardial Ischemia/Reperfusion Injury-Review of Its Significance and the Potential Impact of Therapeutic Interference by C1 Esterase Inhibitor.Frontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Activation of the complement cascade (CC) with myocardial infarction (MI) acutely initiates immune cell infiltration, membrane attack complex formation on injured myocytes, and exacerbates myocardial injury. Recent studies implicate the CC in mobilization of stem/progenitor cells and tissue regeneration. Its role in chronic MI is unknown. Here, we consider complement component C3, in the chronic response to MI. C3 knockout (KO) mice were studied after permanent coronary artery ligation. C3 deficiency exacerbated myocardial dysfunction 28 days after MI compared to WT with further impaired systolic function and LV dilation despite similar infarct size 24 hours post-MI. Morphometric analysis 28 days post-MI showed C3 KO mice had more scar tissue with less viable myocardium within the infarct zone which correlated with decreased c-kit(pos) cardiac stem/progenitor cells (CPSC), decreased proliferating Ki67(pos) CSPCs and decreased formation of new BrdU(pos) /α-sarcomeric actin(pos) myocytes, and increased apoptosis compared to WT. Decreased CSPCs and increased apoptosis were evident 7 days post-MI in C3 KO hearts. The inflammatory response with MI was attenuated in the C3 KO and was accompanied by attenuated hematopoietic, pluripotent, and cardiac stem/progenitor cell mobilization into the peripheral blood 72 hours post-MI. These results are the first to demonstrate that CC, through C3, contributes to myocardial preservation and regeneration in response to chronic MI. Responses in the C3 KO infer that C3 activation in response to MI expands the resident CSPC population, increases new myocyte formation, increases and preserves myocardium, inflammatory response, and bone marrow stem/progenitor cell mobilization to preserve myocardial function.
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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.