ArticleJournal of molecular and cellular cardiology2012
Ca(2+) influx through L-type Ca(2+) channels and transient receptor potential channels activates pathological hypertrophy signaling.
Article in Journal of molecular and cellular cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 89 citations in OpenAlex.
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- Role of RIPK3‑CaMKII‑mPTP signaling pathway‑mediated necroptosis in cardiovascular diseases (Review).International journal of molecular medicine · 2023Review
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- A fully-automated low-cost cardiac monolayer optical mapping robot.Frontiers in cardiovascular medicine · 2023Article
- The SOCE Machinery: An Unbalanced Knowledge between Left and Right Ventricular Pathophysiology.Cells · 2022Review
- (-)-Carvone Modulates Intracellular Calcium Signaling with Antiarrhythmic Action in Rat Hearts.Arquivos brasileiros de cardiologia · 2022Article
- Interaction of background CaThe Journal of physiology · 2022Article
- Kinetic mechanisms by which nickel alters the calcium (CaJournal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2021Article
- Nutraceutical, Dietary, and Lifestyle Options for Prevention and Treatment of Ventricular Hypertrophy and Heart Failure.International journal of molecular sciences · 2021Review
- Secondhand Smoke Exposure Impairs Ion Channel Function and Contractility of Mesenteric Arteries.Function (Oxford, England) · 2021Article
- CaThe Journal of biological chemistry · 2020Article
- TRPC Channels in Cardiac Plasticity.Cells · 2020Review
- Effect of SKF‑96365 on cardiomyocyte hypertrophy induced by angiotensin II.Molecular medicine reports · 2020Article
- Article
- Myocardial-restricted ablation of the GTPase RAD results in a pro-adaptive heart response in mice.The Journal of biological chemistry · 2019Article
- Cardiac-specific overexpression of caveolin-3 preserves t-tubular IExperimental physiology · 2019Article
- The attenuation of myocardial hypertrophy by atorvastatin via the intracellular calcium signal and the p38 MAPK pathway.International journal of clinical and experimental pathology · 2019Article
- Glucocorticoid stimulation increases cardiac contractility by SGK1-dependent SOCE-activation in rat cardiac myocytes.PloS one · 2019Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Common cardiovascular diseases such as hypertension and myocardial infarction require that myocytes develop greater than normal force to maintain cardiac pump function. This requires increases in [Ca(2+)]. These diseases induce cardiac hypertrophy and increases in [Ca(2+)] are known to be an essential proximal signal for activation of hypertrophic genes. However, the source of "hypertrophic" [Ca(2+)] is not known and is the topic of this study. The role of Ca(2+) influx through L-type Ca(2+) channels (LTCC), T-type Ca(2+) channels (TTCC) and transient receptor potential (TRP) channels on the activation of calcineurin (Cn)-nuclear factor of activated T cells (NFAT) signaling and myocyte hypertrophy was studied. Neonatal rat ventricular myocytes (NRVMs) and adult feline ventricular myocytes (AFVMs) were infected with an adenovirus containing NFAT-GFP, to determine factors that could induce NFAT nuclear translocation. Four millimolar Ca(2+) or pacing induced NFAT nuclear translocation. This effect was blocked by Cn inhibitors. In NRVMs Nifedipine (Nif, LTCC antagonist) blocked high Ca(2+)-induced NFAT nuclear translocation while SKF-96365 (TRP channel antagonist) and Nickel (Ni, TTCC antagonist) were less effective. The relative potency of these antagonists against Ca(2+) induced NFAT nuclear translocation (Nif>SKF-96365>Ni) was similar to their effects on Ca(2+) transients and the LTCC current. Infection of NRVM with viruses containing TRP channels also activated NFAT-GFP nuclear translocation and caused myocyte hypertrophy. TRP effects were reduced by SKF-96365, but were more effectively antagonized by Nif. These experiments suggest that Ca(2+) influx through LTCCs is the primary source of Ca(2+) to activate Cn-NFAT signaling in NRVMs and AFVMs. While TRP channels cause hypertrophy, they appear to do so through a mechanism involving Ca(2+) entry via LTCCs.
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