ArticleAmerican journal of physiology. Heart and circulatory physiology2013
Oxidative activation of Ca(2+)/calmodulin-activated kinase II mediates ER stress-induced cardiac dysfunction and apoptosis.
Article in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 45 citations in OpenAlex.
- Angiotensin-(1-9) prevents angiotensin II-induced endothelial apoptosis through CNPY2/PERK pathway.Apoptosis : an international journal on programmed cell death · 2023Article
- CaMKII orchestrates endoplasmic reticulum stress and apoptosis in doxorubicin-induced cardiotoxicity by regulating the IRE1α/XBP1s pathway.Journal of cellular and molecular medicine · 2022Article
- Current Strategies and Potential Prospects for Nanoparticle-Mediated Treatment of Diabetic Nephropathy.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022Review
- Didymin Ameliorates Liver Fibrosis by Alleviating Endoplasmic Reticulum Stress and Glycerophospholipid Metabolism: Based on Transcriptomics and Metabolomics.Drug design, development and therapy · 2022Article
- CaFrontiers in cardiovascular medicine · 2022Article
- CaMKII-δ9 Induces Cardiomyocyte Death to Promote Cardiomyopathy and Heart Failure.Frontiers in cardiovascular medicine · 2021Article
- Knockdown of miR-1275 protects against cardiomyocytes injury through promoting neuromedin U type 1 receptor.Cell cycle (Georgetown, Tex.) · 2020Article
- Taurine attenuates isoproterenol-induced H9c2 cardiomyocytes hypertrophy by improving antioxidative ability and inhibiting calpain-1-mediated apoptosis.Molecular and cellular biochemistry · 2020Article
- Mitochondrial Quality Control: Role in Cardiac Models of Lethal Ischemia-Reperfusion Injury.Cells · 2020Review
- Broken heart: A matter of the endoplasmic reticulum stress bad management?World journal of cardiology · 2019Review
- Selenium-Rich Diet Induces Myocardial Structural and Functional Abnormalities by Activating Caspase-9 and Caspase-3 in Gpx-1P198L-Overexpression Transgenic Mice.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- ALDH2 protects against high fat diet-induced obesity cardiomyopathy and defective autophagy: role of CaM kinase II, histone H3K9 methyltransferase SUV39H, Sirt1, and PGC-1α deacetylation.International journal of obesity (2005) · 2018Article
- Endoplasmic reticulum stress in the heart: insights into mechanisms and drug targets.British journal of pharmacology · 2018Review
- Review
- CaMKII is a nodal signal for multiple programmed cell death pathways in heart.Journal of molecular and cellular cardiology · 2017Review
- mTOR-Independent autophagy inducer trehalose rescues against insulin resistance-induced myocardial contractile anomalies: Role of p38 MAPK and Foxo1.Pharmacological research · 2016Article
- Modulation of P2X4/P2X7/Pannexin-1 sensitivity to extracellular ATP via Ivermectin induces a non-apoptotic and inflammatory form of cancer cell death.Scientific reports · 2015Article
- Regulation of CaMKII signaling in cardiovascular disease.Frontiers in pharmacology · 2015Review
- Effect of ligustilide on Ang II-induced hypertrophy in cardiomyocytes and the potential mechanisms.Experimental and therapeutic medicine · 2014Article
- Heavy metal scavenger metallothionein attenuates ER stress-induced myocardial contractile anomalies: role of autophagy.Toxicology letters · 2014Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Endoplasmic reticulum (ER) stress elicits oxidative stress and intracellular Ca(2+) derangement via activation of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII). This study was designed to examine the role of CaMKII in ER stress-induced cardiac dysfunction and apoptosis as well as the effect of antioxidant catalase. Wild-type FVB and transgenic mice with cardiac-specific overexpression of catalase were challenged with the ER stress inducer tunicamycin (3 mg/kg ip for 48 h). Presence of ER stress was verified using the ER stress protein markers immunoglobulin binding protein (BiP) and C/EBP homologous protein (CHOP), the effect of which was unaffected by catalase overexpression. Echocardiographic assessment revealed that tunicamycin elicited cardiac remodeling (enlarged end-systolic diameter without affecting diastolic and ventricular wall thickness), depressed fractional shortening, ejection fraction, and cardiomyocyte contractile capacity, intracellular Ca(2+) mishandling, accumulation of reactive oxygen species (superoxide production and NADPH oxidase p47phox level), CaMKII oxidation, and apoptosis (evidenced by Bax, Bcl-2/Bax ratio, and TUNEL staining), the effects of which were obliterated by catalase. Interestingly, tunicamycin-induced cardiomyocyte mechanical anomalies and cell death were ablated by the CaMKII inhibitor KN93, in a manner reminiscent of catalase. These data favored a permissive role of oxidative stress and CaMKII activation in ER stress-induced cardiac dysfunction and cell death. Our data further revealed the therapeutic potential of antioxidant or CaMKII inhibition in cardiac pathological conditions associated with ER stress. This research shows for the first time that contractile dysfunction caused by ER stress is a result of the oxidative activation of the CaMKII pathway.
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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.