ArticleThe Journal of clinical investigation2009
Ca2+/calmodulin-dependent kinase II triggers cell membrane injury by inducing complement factor B gene expression in the mouse heart.
Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
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Who cites it
82 citing papers in PubMed, 110 citations in OpenAlex.
- Complement C3c as a biomarker in heart failure.Mediators of inflammation · 2013Trial
- Tumor-derived neutrophil extracellular trap-associated DNA impairs treatment efficacy in breast cancer via CCDC25-dependent epithelial-mesenchymal transition.The Journal of clinical investigation · 2026Article
- Immune checkpoint inhibitor-induced cardiotoxicity: from immune mechanisms to clinical surveillance and targeted therapies.Frontiers in cardiovascular medicine · 2026Review
- LRRC8A drives NADPH oxidase-mediated mitochondrial dysfunction and inflammation in allergic rhinitis.Journal of translational medicine · 2024Article
- Ischemic cardiac stromal fibroblast-derived protein mediators in the infarcted myocardium and transcriptomic profiling at single cell resolution.Functional & integrative genomics · 2024Article
- The Role of Necroptosis in Cerebral Ischemic Stroke.Molecular neurobiology · 2024Review
- CaMKII as a Therapeutic Target in Cardiovascular Disease.Annual review of pharmacology and toxicology · 2023Review
- Splicing and Dicing: A Deeper Dive Into CaMKIIδ and Cardiac Inflammation.Circulation research · 2022Article
- Current Understanding of Molecular Pathophysiology of Heart Failure With Preserved Ejection Fraction.Frontiers in physiology · 2022Review
- Cardioprotection by SGLT2 Inhibitors-Does It All Come Down to NaInternational journal of molecular sciences · 2021Review
- CaMKII oxidation is a critical performance/disease trade-off acquired at the dawn of vertebrate evolution.Nature communications · 2021Article
- Cardioprotective effect of pioglitazone and curcumin against diabetic cardiomyopathy in type 1 diabetes mellitus: impact on CaMKII/NF-κB/TGF-β1 and PPAR-γ signaling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
- CaMKII-δ9 Induces Cardiomyocyte Death to Promote Cardiomyopathy and Heart Failure.Frontiers in cardiovascular medicine · 2021Article
- The Alternative Complement Pathway Is Activated Without a Corresponding Terminal Pathway Activation in Patients With Heart Failure.Frontiers in immunology · 2021Article
- Inverse association between periumbilical fat and longevity mediated by complement C3 and cardiac structure.Aging · 2020Article
- Mitochondrial CaMKII causes adverse metabolic reprogramming and dilated cardiomyopathy.Nature communications · 2020Article
- The molecular mechanisms associated with the physiological responses to inflammation and oxidative stress in cardiovascular diseases.Biophysical reviews · 2020Review
- Loss of myeloid differentiation protein 1 promotes atrial fibrillation in heart failure with preserved ejection fraction.ESC heart failure · 2020Article
- Cardiac CaMKIIEvidence-based complementary and alternative medicine : eCAM · 2020Article
- Tilianin Protects against Ischemia/Reperfusion-Induced Myocardial Injury through the Inhibition of the CaBioMed research international · 2020Article
22 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors at 5 institutions in 1 country.
Funding
Abstract
Myocardial Ca2+/calmodulin-dependent protein kinase II (CaMKII) inhibition improves cardiac function following myocardial infarction (MI), but the CaMKII-dependent pathways that participate in myocardial stress responses are incompletely understood. To address this issue, we sought to determine the transcriptional consequences of myocardial CaMKII inhibition after MI. We performed gene expression profiling in mouse hearts with cardiomyocyte-delimited transgenic expression of either a CaMKII inhibitory peptide (AC3-I) or a scrambled control peptide (AC3-C) following MI. Of the 8,600 mRNAs examined, 156 were substantially modulated by MI, and nearly half of these showed markedly altered responses to MI with CaMKII inhibition. CaMKII inhibition substantially reduced the MI-triggered upregulation of a constellation of proinflammatory genes. We studied 1 of these proinflammatory genes, complement factor B (Cfb), in detail, because complement proteins secreted by cells other than cardiomyocytes can induce sarcolemmal injury during MI. CFB protein expression in cardiomyocytes was triggered by CaMKII activation of the NF-kappaB pathway during both MI and exposure to bacterial endotoxin. CaMKII inhibition suppressed NF-kappaB activity in vitro and in vivo and reduced Cfb expression and sarcolemmal injury. The Cfb-/- mice were partially protected from the adverse consequences of MI. Our findings demonstrate what we believe is a novel target for CaMKII in myocardial injury and suggest that CaMKII is broadly important for the genetic effects of MI in cardiomyocytes.
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