ArticleScientific reports2019
Regulation of Cardiac Mast Cell Maturation and Function by the Neurokinin-1 Receptor in the Fibrotic Heart.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
What it found
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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
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Neurotransmitter and neuropeptide regulation of mast cell function: a systematic review.Journal of neuroinflammation · 2020Pooled it
- Neurokinin-1 receptor activation protects against cardiac fibrosis, inflammation and diastolic dysfunction in type 2 diabetic mice.British journal of pharmacology · 2026Article
- Tachykinin Receptors and their Antagonists: Unraveling Their Role in Metabolic Disorders and Therapeutic Innovations.Current drug targets · 2025Review
- Cellular metabolism of substance P produces neurokinin-1 receptor peptide agonists with diminished cyclic AMP signaling.American journal of physiology. Cell physiology · 2024Article
- Comparative analyses of various IgE-mediated and non-IgE-mediated inducers of mast cell degranulation for in vitro study.Immunologic research · 2024Article
- Advances in the research and application of neurokinin-1 receptor antagonists.Journal of Zhejiang University. Science. B · 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
- Immunomodulatory contribution of mast cells to the regenerative biomaterial microenvironment.NPJ Regenerative medicine · 2023Article
- Histamine receptors in heart failure.Heart failure reviews · 2022Review
- Interactions Between Immunomodulatory Biomaterials and Immune Microenvironment: Cues for Immunomodulation Strategies in Tissue Repair.Frontiers in bioengineering and biotechnology · 2022Review
- Article
- Neurokinin receptors and their implications in various autoimmune diseases.Current research in immunology · 2021Review
- The Histamine 3 Receptor Is Expressed in the Heart and Its Activation Opposes Adverse Cardiac Remodeling in the Angiotensin II Mouse Model.International journal of molecular sciences · 2020Article
- Recent advances in mast cell activation and regulation.F1000Research · 2020Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Cardiac fibrosis is an underlying cause of diastolic dysfunction, contributing to heart failure. Substance P (SP) activation of the neurokinin-1 receptor (NK-1R) contributes to cardiac fibrosis in hypertension. However, based on in vitro experiments, this does not appear to be via direct activation of cardiac fibroblasts. While numerous cells could mediate the fibrotic effects of SP, herein, we investigate mast cells (MC) as a mechanism mediating the fibrotic actions of SP, since MCs are known to play a role in cardiac fibrosis and respond to SP. Spontaneously hypertensive rats (SHR) were treated with the NK-1R antagonist L732138 (5 mg/kg/d) from 8 to 12 weeks of age. L732138 prevented increased MC maturation of resident immature MCs. NK-1R blockade also prevented increased cardiac MC maturation in angiotensin II-infused mice. MC-deficient mice were used to test the importance of MC NK-1Rs to MC activation. MC-deficient mice administered angiotensin II did not develop fibrosis; MC-deficient mice reconstituted with MCs did develop fibrosis. MC-deficient mice reconstituted with MCs lacking the NK-1R also developed fibrosis, indicating that NK-1Rs are not required for MC activation in this setting. In conclusion, the NK-1R causes MC maturation, however, other stimuli are required to activate MCs to cause fibrosis.
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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.