ArticleAmerican journal of physiology. Heart and circulatory physiology2010
{beta}1-Adrenergic receptor activation induces mouse cardiac myocyte death through both L-type calcium channel-dependent and -independent pathways.
Article in American journal of physiology. Heart and circulatory physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 42 citations in OpenAlex.
- A primary isolated heart model of Takotsubo syndrome for mechanistic investigation and preclinical therapeutic testing.European heart journal open · 2026Article
- Aberrant myocardial calcium cycling: pathogenic mechanisms and targeted therapeutics for heart failure.Frontiers in cardiovascular medicine · 2026Review
- Role of cAMP in Cardiomyocyte Viability: Beneficial or Detrimental?Circulation research · 2023Article
- Dopamine, Immunity, and Disease.Pharmacological reviews · 2023Review
- The role of calcium homeostasis remodeling in inherited cardiac arrhythmia syndromes.Pflugers Archiv : European journal of physiology · 2021Review
- CaMKII in Regulation of Cell Death During Myocardial Reperfusion Injury.Frontiers in molecular biosciences · 2021Review
- GRK5 Controls SAP97-Dependent Cardiotoxic βCirculation research · 2020Article
- DRD4 Mitigates Myocardial Ischemia/Reperfusion Injury in Association With PI3K/AKT Mediated Glucose Metabolism.Frontiers in pharmacology · 2020Article
- Toll-like receptor 4-induced ryanodine receptor 2 oxidation and sarcoplasmic reticulum CaThe Journal of biological chemistry · 2018Article
- Dedifferentiation, Proliferation, and Redifferentiation of Adult Mammalian Cardiomyocytes After Ischemic Injury.Circulation · 2017Article
- The expanding GRK interactome: Implications in cardiovascular disease and potential for therapeutic development.Pharmacological research · 2016Review
- CaMKIIδ mediates β-adrenergic effects on RyR2 phosphorylation and SR Ca(2+) leak and the pathophysiological response to chronic β-adrenergic stimulation.Journal of molecular and cellular cardiology · 2015Article
- Mst1 inhibition rescues β1-adrenergic cardiomyopathy by reducing myocyte necrosis and non-myocyte apoptosis rather than myocyte apoptosis.Basic research in cardiology · 2015Article
- Effects of exogenous neurotrophin-3 on myocyte apoptosis and Ca(2+)-ATP enzyme levels following nerve injury in rats.International journal of clinical and experimental medicine · 2015Article
- β-Adrenergic receptor-mediated transactivation of epidermal growth factor receptor decreases cardiomyocyte apoptosis through differential subcellular activation of ERK1/2 and Akt.Journal of molecular and cellular cardiology · 2014Article
- β-adrenergic regulation of the L-type Ca2+ channel does not require phosphorylation of α1C Ser1700.Circulation research · 2013Article
- Mechanical regulation of native and the recombinant calcium channel.Cell calcium · 2013Article
- Ca(2+) influx through L-type Ca(2+) channels and transient receptor potential channels activates pathological hypertrophy signaling.Journal of molecular and cellular cardiology · 2012Article
- Repair of the injured adult heart involves new myocytes potentially derived from resident cardiac stem cells.Circulation research · 2011Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Cardiac diseases persistently increase the contractility demands of cardiac myocytes, which require activation of the sympathetic nervous system and subsequent increases in myocyte Ca(2+) transients. Persistent exposure to sympathetic and/or Ca(2+) stress is associated with myocyte death. This study examined the respective roles of persistent beta-adrenergic receptor (beta-AR) agonist exposure and high Ca(2+) concentration in myocyte death. Ventricular myocytes (VMs) were isolated from transgenic (TG) mice with cardiac-specific and inducible expression of the beta(2a)-subunit of the L-type Ca(2+) channel (LTCC). VMs were cultured, and the rate of myocyte death was measured in the presence of isoproterenol (ISO), other modulators of Ca(2+) handling and the beta-adrenergic system, and inhibitors of caspases and reactive oxygen species generation. The rate of myocyte death was greater in TG vs. wild-type myocytes and accelerated by ISO in both groups, although ISO did not increase LTCC current (I(Ca-L)) in TG-VMs. Nifedipine, an LTCC antagonist, only partially prevented myocyte death. These results suggest both LTCC-dependent and -independent mechanisms in ISO induced myocyte death. ISO increased the contractility of wild type and TG-VMs by enhancing sarcoplasmic reticulum function and inhibiting sarco(endo)plasmic reticulum Ca(2+)-ATPase, Na(+)/Ca(2+) exchanger, and CaMKII partially protected myocyte from death induced by both Ca(2+) and ISO. Caspase and reactive oxygen species inhibitors did not, but beta(2)-AR activation did, reduce myocyte death induced by enhanced I(Ca-L) and ISO stimulation. Our results suggest that catecholamines induce myocyte necrosis primarily through beta(1)-AR-mediated increases in I(Ca-L), but other mechanisms are also involved in rodents.
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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.