ArticleCirculation research2009
TRPC1 channels are critical for hypertrophic signaling in the heart.
Article in Circulation research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.
What it found
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Who cites it
108 citing papers in PubMed, 220 citations in OpenAlex.
- Shear stress-induced CaBiological research · 2026Article
- Research progress on programmed cell death of cardiomyocytes in pressure-overload hypertrophic cardiomyopathy.Apoptosis : an international journal on programmed cell death · 2025Review
- Unlocking the potential of cardiac TRP channels using knockout mice models.Frontiers in physiology · 2025Article
- Mechanosensitive ion channels in glaucoma pathophysiology.Vision research · 2024Review
- High-content method for mechanosignaling studies using IsoStretcher technology and quantitative CaCellular and molecular life sciences : CMLS · 2024Article
- Canonical transient receptor potential channel 1 aggravates myocardial ischemia-and-reperfusion injury by upregulating reactive oxygen species.Journal of pharmaceutical analysis · 2023Article
- Coordinated Metabolic Responses Facilitate Cardiac Growth in Pregnancy and Exercise.Current heart failure reports · 2023Review
- TRP (transient receptor potential) ion channel family: structures, biological functions and therapeutic interventions for diseases.Signal transduction and targeted therapy · 2023Review
- The SOCE Machinery: An Unbalanced Knowledge between Left and Right Ventricular Pathophysiology.Cells · 2022Review
- Cardiac Hypertrophy: From Pathophysiological Mechanisms to Heart Failure Development.Reviews in cardiovascular medicine · 2022Review
- Role of store-operated Ca2+ entry in cardiovascular disease.Cell communication and signaling : CCS · 2022Review
- The Roles of Transient Receptor Potential Ion Channels in Pathologies of Glaucoma.Frontiers in physiology · 2022Review
- TRPC1 channels underlie stretch-modulated sarcoplasmic reticulum calcium leak in cardiomyocytes.Frontiers in physiology · 2022Article
- Basal Vascular Smooth Muscle Cell Tone in eNOS Knockout Mice Can Be Reversed by Cyclic Stretch and Is Independent of Age.Frontiers in physiology · 2022Article
- Fibroblast Growth Factor 23 Stimulates Cardiac Fibroblast Activity through Phospholipase C-Mediated Calcium Signaling.International journal of molecular sciences · 2021Article
- Transcriptional profiles of genes related to electrophysiological function in Scn5aPhysiological reports · 2021Article
- Modulation of the Cardiac Myocyte Action Potential by the Magnesium-Sensitive TRPM6 and TRPM7-like Current.International journal of molecular sciences · 2021Article
- Calcium and Heart Failure: How Did We Get Here and Where Are We Going?International journal of molecular sciences · 2021Review
- Mechanosensitive ion channels in cell migration.Cells & development · 2021Review
- SOCE in the cardiomyocyte: the secret is in the chambers.Pflugers Archiv : European journal of physiology · 2021Review
48 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
rationaleCardiac muscle adapts to increase workload by altering cardiomyocyte size and function resulting in cardiac hypertrophy. G protein-coupled receptor signaling is known to govern the hypertrophic response through the regulation of ion channel activity and downstream signaling in failing cardiomyocytes.
objectiveTransient receptor potential canonical (TRPC) channels are G protein-coupled receptor operated channels previously implicated in cardiac hypertrophy. Our objective of this study is to better understand how TRPC channels influence cardiomyocyte calcium signaling. METHODS AND
resultsHere, we used whole cell patch clamp of adult cardiomyocytes to show upregulation of a nonselective cation current reminiscent of TRPC channels subjected to pressure overload. This TRPC current corresponds to the increased TRPC channel expression noted in hearts of mice subjected to pressure overload. Importantly, we show that mice lacking TRPC1 channels are missing this putative TRPC current. Moreover, Trpc1(-)(/)(-) mice fail to manifest evidence of maladaptive cardiac hypertrophy and maintain preserved cardiac function when subjected to hemodynamic stress and neurohormonal excess. In addition, we provide a mechanistic basis for the protection conferred to Trpc1(-)(/)(-) mice as mechanosensitive signaling through calcineurin/NFAT, mTOR and Akt is altered in Trpc1(-)(/)(-) mice.
conclusionsFrom these studies, we suggest that TRPC1 channels are critical for the adaptation to biomechanical stress and TRPC dysregulation leads to maladaptive cardiac hypertrophy and 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.