ArticleEBioMedicine2018
TRPA1 inhibition ameliorates pressure overload-induced cardiac hypertrophy and fibrosis in mice.
Article in EBioMedicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed.
- Systolic pressure overload caused pulmonary oxidative stress, vessel remodeling and severe microvascular thrombosis in CD40 knockout mice through promoting platelet aggregation.Redox biology · 2026Article
- Transient receptor potential ankyrin 1 promotes the expression of interferon-stimulated antiviral genes in human A549 lung epithelial cells.Molecular pharmacology · 2026Article
- Article
- Leucine-Rich Repeat-Containing G Protein-Coupled Receptor 6 Ameliorates Pressure Overload-Induced Cardiac Hypertrophy by Regulating Cardiomyocyte Metabolic Reprogramming.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- CaBiomedicines · 2025Review
- PRMT1 alleviates isoprenaline-induced myocardial hypertrophy by methylating SRSF1.Acta biochimica et biophysica Sinica · 2024Article
- Resolvin D2/GPR 18 axis ameliorates pressure overload-induced heart failure by inhibiting pro-inflammatory macrophage polarization.Journal of lipid research · 2024Article
- 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
- Single-cell transcriptomics reveals writers of RNA modification-mediated immune microenvironment and cardiac resident Macro-MYL2 macrophages in heart failure.BMC cardiovascular disorders · 2024Article
- Role of transient receptor potential ankyrin 1 in idiopathic pulmonary fibrosis: modulation of M2 macrophage polarization.Cellular and molecular life sciences : CMLS · 2024Article
- Epidermal Growth Factor-Like Repeats and Discoidin I-Like Domains 3 Deficiency Attenuates Dilated Cardiomyopathy by Inhibiting Ubiquitin Specific Peptidase 10 Dependent Smad4 Deubiquitination.Journal of the American Heart Association · 2024Article
- Article
- Discovery of PRDM16-Mediated TRPA1 Induction as the Mechanism for Low Tubulo-Interstitial Fibrosis in Diabetic Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Possible mechanisms of SARS-CoV-2-associated myocardial fibrosis: reflections in the post-pandemic era.Frontiers in microbiology · 2024Review
- Unveiling the role of TRPA1 in cardiovascular health and disease: a mini review.Frontiers in cardiovascular medicine · 2024Review
- Transcriptomic profile of the mechanosensitive ion channelome in human cardiac fibroblasts.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- Macrophage neogenin deficiency exacerbates myocardial remodeling and inflammation after acute myocardial infarction through JAK1-STAT1 signaling.Cellular and molecular life sciences : CMLS · 2023Article
- TRPA1 promotes cisplatin-induced acute kidney injury via regulating the endoplasmic reticulum stress-mitochondrial damage.Journal of translational medicine · 2023Article
- Activation of TRPA1 in Bladder Suburothelial Myofibroblasts Counteracts TGF-β1-Induced Fibrotic Changes.International journal of molecular sciences · 2023Article
- The emerging role of leptin in obesity-associated cardiac fibrosis: evidence and mechanism.Molecular and cellular biochemistry · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRecent evidence has indicated that the transient receptor potential ankyrin 1 (TRPA1) is expressed in the cardiovascular system and implicated in the development and progression of several cardiovascular diseases. However, the effects of TRPA1 on cardiac hypertrophy development remain unclear. The aim of this study was to determine the role of TRPA1 in cardiac hypertrophy and fibrosis development.
methodsC57BL/6J mice were subjected to transverse aortic constriction (TAC) and were orally treated with the TRPA1 selective inhibitors HC-030031 (HC) and TCS-5861528 (TCS). Morphological assessments, echocardiographic parameters, histological analyses and flow cytometry were used to evaluate cardiac hypertrophy and fibrosis.
resultsHuman and mouse hypertrophic hearts presented with noticeably increased TRPA1 protein levels. Inhibition of TRPA1 by HC and TCS attenuated cardiac hypertrophy and preserved cardiac function after chronic pressure overload, as evidenced by increased heart weight/body weight ratio, cardiomyocyte cross-sectional area and mRNA expression of hypertrophic markers, including ANP, BNP and β-MHC. Dramatic interstitial fibrosis was observed in the mice subjected to TAC surgery, and this was markedly attenuated in the HC and TCS treated mice. Mechanistically, the results revealed that TRPA1 inhibition ameliorated pressure overload-induced cardiac hypertrophy by negatively regulating Ca
conclusionsTRPA1 inhibition protected against cardiac hypertrophy and suppressed cardiac dysfunction via Ca
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