ArticleJournal of molecular and cellular cardiology2011
Calcium influx through Cav1.2 is a proximal signal for pathological cardiomyocyte hypertrophy.
Article in Journal of molecular and cellular cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed, 110 citations in OpenAlex.
- Histamine N-methyltransferase upregulation, cardiac hypertrophy, and heart failure.European heart journal · 2026Article
- Voltage-gated calcium channels generate blastema Ca2+ fluxes restraining zebrafish fin regenerative outgrowth.Development (Cambridge, England) · 2025Article
- Cell size induced bias of current density in hypertrophic cardiomyocytes.Channels (Austin, Tex.) · 2024Article
- Protein Kinase A Is a Master Regulator of Physiological and Pathological Cardiac Hypertrophy.Circulation research · 2024Article
- Dysregulated Rbfox2 produces aberrant splicing of CaCardiovascular diabetology · 2023Article
- Calcium Handling Remodeling Underlies Impaired Sympathetic Stress Response in Ventricular Myocardium fromInternational journal of molecular sciences · 2023Article
- Calcium "stress" adds a third hit in driving heart failure with preserved ejection fraction.American journal of physiology. Heart and circulatory physiology · 2023Article
- Combining three independent pathological stressors induces a heart failure with preserved ejection fraction phenotype.American journal of physiology. Heart and circulatory physiology · 2023Article
- Modulation of CaHandbook of experimental pharmacology · 2023Article
- β subunits of voltage-gated calcium channels in cardiovascular diseases.Frontiers in cardiovascular medicine · 2023Review
- Adrenergic Regulation of Calcium Channels in the Heart.Annual review of physiology · 2022Review
- Shexiang Baoxin Pills Could Alleviate Isoproterenol-Induced Heart Failure Probably through its Inhibition of CaV1.2 Calcium Channel Currents.Biochemistry research international · 2022Article
- L-type channel inactivation balances the increased peak calcium current due to absence of Rad in cardiomyocytes.The Journal of general physiology · 2021Article
- Influence of miR-221/222 on cardiomyocyte calcium handling and function.Cell & bioscience · 2021Article
- The CaeLife · 2021Article
- The mineralocorticoid receptor leads to increased expression of EGFR and T-type calcium channels that support HL-1 cell hypertrophy.Scientific reports · 2021Article
- Nucleoplasmic CaCirculation research · 2021Article
- The βFrontiers in cardiovascular medicine · 2021Article
- A low voltage activated CaChannels (Austin, Tex.) · 2020Article
- The CaMKII phosphorylation site Thr1604 in the CaChannels (Austin, Tex.) · 2020Article
7 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
Pathological cardiac hypertrophy (PCH) is associated with the development of arrhythmia and congestive heart failure. While calcium (Ca(2+)) is implicated in hypertrophic signaling pathways, the specific role of Ca(2+) influx through the L-type Ca(2+) channel (I(Ca-L)) has been controversial and is the topic of this study. To determine if and how sustained increases in I(Ca-L) induce PCH, transgenic mouse models with low (LE) and high (HE) expression levels of the β2a subunit of Ca(2+) channels (β2a) and in cultured adult feline (AF) and neonatal rat (NR) ventricular myocytes (VMs) infected with an adenovirus containing a β2a-GFP were used. In vivo, β2a LE and HE mice had increased heart weight to body weight ratio, posterior wall and interventricular septal thickness, tissue fibrosis, myocyte volume, and cross-sectional area and the expression of PCH markers in a time- and dose-dependent manner. PCH was associated with a hypercontractile phenotype including enhanced I(Ca-L), fractional shortening, peak Ca(2+) transient, at the myocyte level, greater ejection fraction, and fractional shortening at the organ level. In addition, LE mice had an exaggerated hypertrophic response to transverse aortic constriction. In vitro overexpression of β2a in cultured AFVMs increased I(Ca-L), cell volume, protein synthesis, NFAT, and HDAC translocations and in NRVMs increased surface area. These effects were abolished by the blockade of I(Ca-L), intracellular Ca(2+), calcineurin, CaMKII, and SERCA. In conclusion, increasing I(Ca-L) is sufficient to induce PCH through the calcineurin/NFAT and CaMKII/HDAC pathways. Both cytosolic and SR/ER-nuclear envelop Ca(2+) pools were shown to be involved.
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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.