ArticleScientific reports2017
TRPC6 counteracts TRPC3-Nox2 protein complex leading to attenuation of hyperglycemia-induced heart failure in mice.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- Review
- The Potential Connection Between Mechanical Stress and Heart Failure with Preserved Ejection Fraction: Mechanistic Insights and Therapeutic Potential.International journal of medical sciences · 2026Review
- Genetic ablation of TRPC6 facilitated age-dependent atherosclerosis progression in an ApoE-/- mouse model.Frontiers in physiology · 2026Article
- Induction of ER stress-mediated apoptosis in breast cancer cell line by the powerful alkylating agent bendamustine and insights into its molecular mechanisms.Medical oncology (Northwood, London, England) · 2025Article
- Modulation of Redox-Sensitive Cardiac Ion Channels.Antioxidants (Basel, Switzerland) · 2025Review
- TRPV2 mediates stress resilience in mouse cardiomyocytes.Communications biology · 2025Article
- Pathophysiological significance and modulation of the transient receptor potential canonical 3 ion channel.Medicinal research reviews · 2024Review
- Article
- Pharmacological Activation of TRPC6 Channel Prevents Colitis Progression.International journal of molecular sciences · 2024Article
- The odyssey of the TR(i)P journey to the cellular membrane.Frontiers in cell and developmental biology · 2024Review
- Myocardial TRPC6-mediated ZnNature communications · 2022Article
- TRPC6, a therapeutic target for pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Moderate Aerobic Training Inhibits Middle-Aged Induced Cardiac Calcineurin-NFAT Signaling by Improving TGF-ß, NPR-A, SERCA2, and TRPC6 in Wistar Rats.Cell journal · 2021Article
- Fibrosis of the diabetic heart: Clinical significance, molecular mechanisms, and therapeutic opportunities.Advanced drug delivery reviews · 2021Review
- Channelling the Force to Reprogram the Matrix: Mechanosensitive Ion Channels in Cardiac Fibroblasts.Cells · 2021Review
- Trpc6 Promotes Doxorubicin-Induced Cardiomyopathy in Male Mice With Pleiotropic Differences Between Males and Females.Frontiers in cardiovascular medicine · 2021Article
- Review
- TRPC Channels in Cardiac Plasticity.Cells · 2020Review
- TRPC Channels: Dysregulation and CaCells · 2020Review
- Canonical Transient Receptor Potential Channels and Vascular Smooth Muscle Cell Plasticity.Journal of lipid and atherosclerosis · 2020Review
Corrections and comments
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Authors and funding
11 authors at 7 institutions in 3 countries.
Funding
Abstract
Excess production of reactive oxygen species (ROS) caused by hyperglycemia is a major risk factor for heart failure. We previously reported that transient receptor potential canonical 3 (TRPC3) channel mediates pressure overload-induced maladaptive cardiac fibrosis by forming stably functional complex with NADPH oxidase 2 (Nox2). Although TRPC3 has been long suggested to form hetero-multimer channels with TRPC6 and function as diacylglycerol-activated cation channels coordinately, the role of TRPC6 in heart is still obscure. We here demonstrated that deletion of TRPC6 had no impact on pressure overload-induced heart failure despite inhibiting interstitial fibrosis in mice. TRPC6-deficient mouse hearts 1 week after transverse aortic constriction showed comparable increases in fibrotic gene expressions and ROS production but promoted inductions of inflammatory cytokines, compared to wild type hearts. Treatment of TRPC6-deficient mice with streptozotocin caused severe reduction of cardiac contractility with enhancing urinary and cardiac lipid peroxide levels, compared to wild type and TRPC3-deficient mice. Knockdown of TRPC6, but not TRPC3, enhanced basal expression levels of cytokines in rat cardiomyocytes. TRPC6 could interact with Nox2, but the abundance of TRPC6 was inversely correlated with that of Nox2. These results strongly suggest that Nox2 destabilization through disrupting TRPC3-Nox2 complex underlies attenuation of hyperglycemia-induced heart failure by TRPC6.
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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.