ArticleCirculation research2009
The Ca(v)3.2 T-type Ca(2+) channel is required for pressure overload-induced cardiac hypertrophy in mice.
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 77 papers.
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Who cites it
77 citing papers in PubMed, 155 citations in OpenAlex.
- Differential contribution of T-type voltage-gated calcium channels to vascular reactivity in the aorta and renal artery of healthy rabbits.Experimental physiology · 2026Article
- Research progress on programmed cell death of cardiomyocytes in pressure-overload hypertrophic cardiomyopathy.Apoptosis : an international journal on programmed cell death · 2025Review
- Degradation of voltage-gated calcium channels: mechanisms and applications in neurological and cardiovascular diseases.Cell communication and signaling : CCS · 2025Review
- Cardiac structural and molecular alterations in rodent models of temporal lobe epilepsy.Epilepsia open · 2025Article
- Updates on Intrinsic Medicinal Chemistry of 1,4-dihydropyridines, Perspectives on Synthesis and Pharmacokinetics of Novel 1,4-dihydropyrimidines as Calcium Channel Blockers: Clinical Pharmacology.Current topics in medicinal chemistry · 2025Review
- Article
- Structure-Function Studies of Sponge-Derived Compounds on the Cardiac CaInternational journal of molecular sciences · 2023Article
- Similarities and Differences between the Orai1 Variants: Orai1α and Orai1β.International journal of molecular sciences · 2022Review
- Multiomic analyses reveal enriched glycolytic processes in β-myosin heavy chain-expressed cardiomyocytes in early cardiac hypertrophy.Journal of molecular and cellular cardiology plus · 2022Article
- T-Type Calcium Channels: A Mixed Blessing.International journal of molecular sciences · 2022Review
- CaJournal of thrombosis and haemostasis : JTH · 2022Article
- Atypically Shaped Cardiomyocytes (ACMs): The Identification, Characterization and New Insights into a Subpopulation of Cardiomyocytes.Biomolecules · 2022Review
- Evidence for a Physiological Role of T-Type Ca Channels in Ventricular Cardiomyocytes of Adult Mice.Membranes · 2022Article
- Article
- The Tarantula Toxin ω-Avsp1a Specifically Inhibits Human CaBiomedicines · 2022Article
- CaPflugers Archiv : European journal of physiology · 2022Review
- The mineralocorticoid receptor leads to increased expression of EGFR and T-type calcium channels that support HL-1 cell hypertrophy.Scientific reports · 2021Article
- Enhanced CaProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Id2 Represses Aldosterone-Stimulated Cardiac T-Type Calcium Channels Expression.International journal of molecular sciences · 2021Article
- Cardiac Gq Receptors and Calcineurin Activation Are Not Required for the Hypertrophic Response to Mechanical Left Ventricular Pressure Overload.Frontiers in cell and developmental biology · 2021Article
17 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Voltage-gated T-type Ca(2+) channels (T-channels) are normally expressed during embryonic development in ventricular myocytes but are undetectable in adult ventricular myocytes. Interestingly, T-channels are reexpressed in hypertrophied or failing hearts. It is unclear whether T-channels play a role in the pathogenesis of cardiomyopathy and what the mechanism might be. Here we show that the alpha(1H) voltage-gated T-type Ca(2+) channel (Ca(v)3.2) is involved in the pathogenesis of cardiac hypertrophy via the activation of calcineurin/nuclear factor of activated T cells (NFAT) pathway. Specifically, pressure overload-induced hypertrophy was severely suppressed in mice deficient for Ca(v)3.2 (Ca(v)3.2(-/-)) but not in mice deficient for Ca(v)3.1 (Ca(v)3.1(-/-)). Angiotensin II-induced cardiac hypertrophy was also suppressed in Ca(v)3.2(-/-) mice. Consistent with these findings, cultured neonatal myocytes isolated from Ca(v)3.2(-/-) mice fail to respond hypertrophic stimulation by treatment with angiotensin II. Together, these results demonstrate the importance of Ca(v)3.2 in the development of cardiac hypertrophy both in vitro and in vivo. To test whether Ca(v)3.2 mediates the hypertrophic response through the calcineurin/NFAT pathway, we generated Ca(v)3.2(-/-), NFAT-luciferase reporter mice and showed that NFAT-luciferase reporter activity failed to increase after pressure overload in the Ca(v)3.2(-/-)/NFAT-Luc mice. Our results provide strong genetic evidence that Ca(v)3.2 indeed plays a pivotal role in the induction of calcineurin/NFAT hypertrophic signaling and is crucial for the activation of pathological cardiac hypertrophy.
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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.