ArticleThe Journal of experimental medicine2016
Mast cells regulate myofilament calcium sensitization and heart function after myocardial infarction.
Article in The Journal of experimental medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
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Who cites it
75 citing papers in PubMed, 112 citations in OpenAlex.
- CD34Histology and histopathology · 2026Review
- T Cell Receptor Repertoires Across the Continuum of Vascular, Myocardial, and Age-Related Diseases.Immunological reviews · 2026Review
- Review
- Targeting Cdc42: Novel Approaches in Cardiovascular Disorders.Current protein & peptide science · 2026Review
- Endothelial Cell Heterogeneity in Carotid Plaque Calcification: An Exploratory Single-Cell Transcriptomic Study with Proteomic Support.International journal of general medicine · 2026Article
- Inflammaging and Senescence-Driven Extracellular Matrix Remodeling in Age-Associated Cardiovascular Disease.Biomolecules · 2025Review
- Role of Mast Cells in Human Health and Disease: Controversies and Novel Therapies.International journal of molecular sciences · 2025Review
- Targeting NLRP3 inflammasome attenuates cardiac pyroptosis and fibrosis in estrogen-deficient diabetic rats.Pflugers Archiv : European journal of physiology · 2025Article
- Immune cell dynamics in heart failure: implicated mechanisms and therapeutic targets.ESC heart failure · 2025Review
- Post-myocardial Infarction Cardiac Remodeling: Multidimensional Mechanisms and Clinical Prospects of Stem Cell Therapy.Stem cell reviews and reports · 2025Review
- The efferocytosis process in aging: Supporting evidence, mechanisms, and therapeutic prospects for age-related diseases.Journal of advanced research · 2025Review
- Complex regulation of cardiac fibrosis: insights from immune cells and signaling pathways.Journal of translational medicine · 2025Review
- Tryptase as a Biomarker for Adverse Prognosis in ST-Segment Elevation Myocardial Infarction Patients: A Prospective Cohort Study.Journal of inflammation research · 2025Article
- Mast cells: a novel therapeutic avenue for cardiovascular diseases?Cardiovascular research · 2024Review
- Uncovering hub genes and immunological characteristics for heart failure utilizing RRA, WGCNA and Machine learning.International journal of cardiology. Heart & vasculature · 2024Article
- Cardiac cell senescence: molecular mechanisms, key proteins and therapeutic targets.Cell death discovery · 2024Review
- Mast Cells in Cardiac Remodeling: Focus on the Right Ventricle.Journal of cardiovascular development and disease · 2024Review
- Cardiac fibrogenesis: an immuno-metabolic perspective.Frontiers in physiology · 2024Review
- Identification of Shared Signature Genes and Immune Microenvironment Subtypes for Heart Failure and Chronic Kidney Disease Based on Machine Learning.Journal of inflammation research · 2024Article
- Early-life interactions between the microbiota and immune system: impact on immune system development and atopic disease.Nature reviews. Immunology · 2023Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
27 authors at 6 institutions in 4 countries.
Funding
Abstract
Acute myocardial infarction (MI) is a severe ischemic disease responsible for heart failure and sudden death. Inflammatory cells orchestrate postischemic cardiac remodeling after MI. Studies using mice with defective mast/stem cell growth factor receptor c-Kit have suggested key roles for mast cells (MCs) in postischemic cardiac remodeling. Because c-Kit mutations affect multiple cell types of both immune and nonimmune origin, we addressed the impact of MCs on cardiac function after MI, using the c-Kit-independent MC-deficient (Cpa3(Cre/+)) mice. In response to MI, MC progenitors originated primarily from white adipose tissue, infiltrated the heart, and differentiated into mature MCs. MC deficiency led to reduced postischemic cardiac function and depressed cardiomyocyte contractility caused by myofilament Ca(2+) desensitization. This effect correlated with increased protein kinase A (PKA) activity and hyperphosphorylation of its targets, troponin I and myosin-binding protein C. MC-specific tryptase was identified to regulate PKA activity in cardiomyocytes via protease-activated receptor 2 proteolysis. This work reveals a novel function for cardiac MCs modulating cardiomyocyte contractility via alteration of PKA-regulated force-Ca(2+) interactions in response to MI. Identification of this MC-cardiomyocyte cross-talk provides new insights on the cellular and molecular mechanisms regulating the cardiac contractile machinery and a novel platform for therapeutically addressable regulators.
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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.