ArticlePloS one2007
TrpC3 regulates hypertrophy-associated gene expression without affecting myocyte beating or cell size.
Article in PloS one, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 57 citations in OpenAlex.
- Unlocking the potential of cardiac TRP channels using knockout mice models.Frontiers in physiology · 2025Article
- The odyssey of the TR(i)P journey to the cellular membrane.Frontiers in cell and developmental biology · 2024Review
- Stretching Promotes Wound Contraction Through Enhanced Expression of Endothelin Receptor B and TRPC3 in Fibroblasts.Plastic and reconstructive surgery. Global open · 2023Article
- The SOCE Machinery: An Unbalanced Knowledge between Left and Right Ventricular Pathophysiology.Cells · 2022Review
- Targeting CaFrontiers in physiology · 2020Review
- Transient receptor potential channels in cardiac health and disease.Nature reviews. Cardiology · 2019Review
- TRP Channels: Current Perspectives in the Adverse Cardiac Remodeling.Frontiers in physiology · 2019Review
- TRPC3 Channels in Cardiac Fibrosis.Frontiers in cardiovascular medicine · 2017Review
- Resistance to pathologic cardiac hypertrophy and reduced expression of CaV1.2 in Trpc3-depleted mice.Molecular and cellular biochemistry · 2016Article
- TRPC4α and TRPC4β Similarly Affect Neonatal Cardiomyocyte Survival during Chronic GPCR Stimulation.PloS one · 2016Article
- Murine cardiac growth, TRPC channels, and cGMP kinase I.Pflugers Archiv : European journal of physiology · 2015Article
- Evidence of a Role for Fibroblast Transient Receptor Potential Canonical 3 Ca2+ Channel in Renal Fibrosis.Journal of the American Society of Nephrology : JASN · 2015Article
- TRPC3 contributes to regulation of cardiac contractility and arrhythmogenesis by dynamic interaction with NCX1.Cardiovascular research · 2015Article
- Role of TRP channels in the cardiovascular system.American journal of physiology. Heart and circulatory physiology · 2015Review
- Activation of transient receptor potential canonical 3 (TRPC3)-mediated Ca2+ entry by A1 adenosine receptor in cardiomyocytes disturbs atrioventricular conduction.The Journal of biological chemistry · 2012Article
- A pathogenic C terminus-truncated polycystin-2 mutant enhances receptor-activated Ca2+ entry via association with TRPC3 and TRPC7.The Journal of biological chemistry · 2009Article
- TRPC1 channels are critical for hypertrophic signaling in the heart.Circulation research · 2009Article
- Selective and direct inhibition of TRPC3 channels underlies biological activities of a pyrazole compound.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Roles of TRP channels in the development of cardiac hypertrophy.Naunyn-Schmiedeberg's archives of pharmacology · 2008Review
- Usefulness of myocardial performance index and biochemical markers for early detection of anthracycline-induced cardiotoxicity in adults.Clinical research in cardiology : official journal of the German Cardiac Society · 2008Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Pathological cardiac hypertrophy is associated with an increased risk of heart failure and cardiovascular mortality. Calcium (Ca(2+)) -regulated gene expression is essential for the induction of hypertrophy, but it is not known how myocytes distinguish between the Ca(2+) signals that regulate contraction and those that lead to cardiac hypertrophy. We used in vitro neonatal rat ventricular myocytes to perform an RNA interference (RNAi) screen for ion channels that mediate Ca(2+)-dependent gene expression in response to hypertrophic stimuli. We identified several ion channels that are linked to hypertrophic gene expression, including transient receptor potential C3 (TrpC3). RNAi-mediated knockdown of TrpC3 decreases expression of hypertrophy-associated genes such as the A- and B-type natriuretic peptides (ANP and BNP) in response to numerous hypertrophic stimuli, while TrpC3 overexpression increases BNP expression. Furthermore, stimuli that induce hypertrophy dramatically increase TrpC3 mRNA levels. Importantly, whereas TrpC3-knockdown strongly reduces gene expression associated with hypertrophy, it has a negligible effect on cell size and on myocyte beating. These results suggest that Ca(2+) influx through TrpC3 channels increases transcription of genes associated with hypertrophy but does not regulate the signaling pathways that control cell size or contraction. Thus TrpC3 may represent an important therapeutic target for the treatment of cardiac hypertrophy and heart failure.
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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.