ReviewFrontiers in cell and developmental biology2021
Innate Immune Cells in Pressure Overload-Induced Cardiac Hypertrophy and Remodeling.
Review in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 47 citations in OpenAlex.
- Histone Deacetylase 7 protects against pathologic cardiac hypertrophy.Journal of molecular and cellular cardiology · 2026Article
- Heterogeneous Myocardial Adaptation to Pressure Overload Reveals a Spared, Vulnerable Segment Identified by Multiparametric Cardiac MRI.NMR in biomedicine · 2026Article
- Diabetic cardiomyopathy: Mechanistic insights on molecular pathways and emerging therapeutic approaches.Heart failure reviews · 2025Review
- Emerging role of the cGAS-STING pathway in cardiovascular diseases: biologic function, mechanisms and targeted therapy.Molecular medicine (Cambridge, Mass.) · 2025Review
- Causal analysis of 731 immunophenotypes and heart failure: A bidirectional Mendelian randomization study.Medicine · 2025Article
- Sex-dependent alterations in cardiac cytochrome P450-mediated arachidonic acid metabolism in pressure overload-induced cardiac hypertrophy in rats.Drug metabolism and disposition: the biological fate of chemicals · 2025Article
- Single-cell RNA sequencing reveals that myeloid S100A8/A9 is a novel regulator of the transition from adaptive hypertrophy to heart failure after pressure overload.Theranostics · 2025Article
- Mast Cells Contribute to Pressure Overload-Induced Myocardial Hypertrophy by Upregulating TRPV4 via Histamine: Role of Ca2+/ CnA/NFATc3 Signaling Pathway.Current medical science · 2024Article
- Large animal models of pressure overload-induced cardiac left ventricular hypertrophy to study remodelling of the human heart with aortic stenosis.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
- Mechanical overload-induced release of extracellular mitochondrial particles from tendon cells leads to inflammation in tendinopathy.Experimental & molecular medicine · 2024Article
- Cardiomyopathy in cirrhosis: From pathophysiology to clinical care.JHEP reports : innovation in hepatology · 2024Review
- TAK1 Activation by NLRP3 Deficiency Confers Cardioprotection Against Pressure Overload-Induced Cardiomyocyte Pyroptosis and Hypertrophy.JACC. Basic to translational science · 2023Article
- A network medicine approach to study comorbidities in heart failure with preserved ejection fraction.BMC medicine · 2023Article
- Review
- The emerging role of leptin in obesity-associated cardiac fibrosis: evidence and mechanism.Molecular and cellular biochemistry · 2023Review
- Eosinophils protect pressure overload- and β-adrenoreceptor agonist-induced cardiac hypertrophy.Cardiovascular research · 2023Article
- Subtyping based on immune cell fractions reveal heterogeneity of cardiac fibrosis in end-stage heart failure.Frontiers in immunology · 2023Article
- Toll-like receptors in cardiac hypertrophy.Frontiers in cardiovascular medicine · 2023Review
- Machine learning-based investigation of the relationship between immune status and left ventricular hypertrophy in patients with end-stage kidney disease.Frontiers in cardiovascular medicine · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
Pressure overload and heart failure are among the leading causes of cardiovascular morbidity and mortality. Accumulating evidence suggests that inflammatory cell activation and release of inflammatory mediators are of vital importance during the pathogenesis of these cardiac diseases. Yet, the roles of innate immune cells and subsequent inflammatory events in these processes remain poorly understood. Here, we outline the possible underlying mechanisms of innate immune cell participation, including mast cells, macrophages, monocytes, neutrophils, dendritic cells, eosinophils, and natural killer T cells in these pathological processes. Although these cells accumulate in the atrium or ventricles at different time points after pressure overload, their cardioprotective or cardiodestructive activities differ from each other. Among them, mast cells, neutrophils, and dendritic cells exert detrimental function in experimental models, whereas eosinophils and natural killer T cells display cardioprotective activities. Depending on their subsets, macrophages and monocytes may exacerbate cardiodysfunction or negatively regulate cardiac hypertrophy and remodeling. Pressure overload stimulates the secretion of cytokines, chemokines, and growth factors from innate immune cells and even resident cardiomyocytes that together assist innate immune cell infiltration into injured heart. These infiltrates are involved in pro-hypertrophic events and cardiac fibroblast activation. Immune regulation of cardiac innate immune cells becomes a promising therapeutic approach in experimental cardiac disease treatment, highlighting the significance of their clinical evaluation in humans.
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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.