ArticleAmerican journal of physiology. Heart and circulatory physiology2013
Cardiomyocyte-specific p65 NF-κB deletion protects the injured heart by preservation of calcium handling.
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 33 papers.
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Who cites it
33 citing papers in PubMed, 56 citations in OpenAlex.
- Challenges in Developing a Microglial NF-Kappa B Conditional Mouse Model for Glioblastoma Studies.Cells · 2026Article
- GLP-1 Receptor Agonists in Heart Failure.Biomolecules · 2025Review
- Peptidylarginine deiminase 4 deficiency alleviates hypoxia/reoxygenation-induced cardiomyocyte injury.PloS one · 2025Article
- Repair of the Infarcted Heart: Cellular Effectors, Molecular Mechanisms and Therapeutic Opportunities.Circulation research · 2024Review
- Growth/differentiation factor 15 (GDF15) expression in the heart after myocardial infarction and cardioprotective effect of pre-ischemic rGDF15 administration.Scientific reports · 2024Article
- Production of a p65Innate immunity · 2023Article
- Inflammation in Myocardial Ischemia/Reperfusion Injury: Underlying Mechanisms and Therapeutic Potential.Antioxidants (Basel, Switzerland) · 2023Review
- RELA governs a network of islet-specific metabolic genes necessary for beta cell function.Diabetologia · 2023Article
- Advanced glycation end products modulate electrophysiological remodeling of right ventricular outflow tract cardiomyocytes: A novel target for diabetes-related ventricular arrhythmogenesis.Physiological reports · 2022Article
- E-cigarette aerosol exacerbates cardiovascular oxidative stress in mice with an inactive aldehyde dehydrogenase 2 enzyme.Redox biology · 2022Article
- Ventricular TLR4 Levels Abrogate TLR2-Mediated Adverse Cardiac Remodeling upon Pressure Overload in Mice.International journal of molecular sciences · 2021Article
- Loss of exosomal LncRNA HCG15 prevents acute myocardial ischemic injury through the NF-κB/p65 and p38 pathways.Cell death & disease · 2021Article
- Post-ischemic Myocardial Inflammatory Response: A Complex and Dynamic Process Susceptible to Immunomodulatory Therapies.Frontiers in cardiovascular medicine · 2021Review
- Cathepsin B aggravated doxorubicin‑induced myocardial injury via NF‑κB signalling.Molecular medicine reports · 2020Article
- NFκB promotes oxidative stress-induced necrosis and ischemia/reperfusion injury by inhibiting Nrf2-ARE pathway.Free radical biology & medicine · 2020Article
- A miR-1275 mimic protects myocardiocyte apoptosis by regulating the Wnt/NF-κB pathway in a rat model of myocardial ischemia-reperfusion-induced myocardial injury.Molecular and cellular biochemistry · 2020Article
- Lactate Suppresses Macrophage Pro-Inflammatory Response to LPS Stimulation by Inhibition of YAP and NF-κB ActivationFrontiers in immunology · 2020Article
- Ischemic postconditioning reduced myocardial ischemia-reperfusion injury: The roles of melatonin and uncoupling protein 3.Anatolian journal of cardiology · 2020Article
- Damage-Associated Molecular Patterns in Myocardial Infarction and Heart Transplantation: The Road to Translational Success.Frontiers in immunology · 2020Review
- Severe T-System Remodeling in Pediatric Viral Myocarditis.Frontiers in cardiovascular medicine · 2020Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
NF-κB is a well-known transcription factor that is intimately involved with inflammation and immunity. We have previously shown that NF-κB promotes inflammatory events and mediates adverse cardiac remodeling following ischemia reperfusion (I/R). Conversely, others have pointed to the beneficial influence of NF-κB in I/R injury related to its anti-apoptotic effects. Understanding the seemingly disparate influence of manipulating NF-κB is hindered, in part, by current approaches that only indirectly interfere with the function of its most transcriptionally active unit, p65 NF-κB. Mice were generated with cardiomyocyte-specific deletion of p65 NF-κB. Phenotypically, these mice and their hearts appeared normal. Basal and stimulated p65 expression were significantly reduced in whole hearts and completely ablated in isolated cardiomyocytes. When compared with wild-type mice, transgenic animals were protected from both global I/R by Langendorff as well as regional I/R by coronary ligation and release. The protected, transgenic hearts had less cytokine activity and decreased apoptosis. Furthermore, p65 ablation was associated with enhanced calcium reuptake by the sarcoplasmic reticulum. This influence on calcium handling was related to increased expression of phosphorylated phospholamban in conditional p65 null mice. In conclusion, cardiomyocyte-specific deletion of the most active, canonical NF-κB subunit affords cardioprotection to both global and regional I/R injury. The beneficial effects of NF-κB inhibition are related, in part, to modulation of intracellular calcium homeostasis.
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