ArticleThe American journal of pathology2007
Tissue-specific effects of the nuclear factor kappaB subunit p50 on myocardial ischemia-reperfusion injury.
Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 68 citations in OpenAlex.
- Discovering new hub genes of dilated cardiomyopathy.ESC heart failure · 2025Article
- Review
- Repair of the Infarcted Heart: Cellular Effectors, Molecular Mechanisms and Therapeutic Opportunities.Circulation research · 2024Review
- Inflammation in Myocardial Ischemia/Reperfusion Injury: Underlying Mechanisms and Therapeutic Potential.Antioxidants (Basel, Switzerland) · 2023Review
- Fibroblast-specific IKK-β deficiency ameliorates angiotensin II-induced adverse cardiac remodeling in mice.JCI insight · 2021Article
- Chemokines in Myocardial Infarction.Journal of cardiovascular translational research · 2021Review
- LncRNA A2M-AS1 lessens the injury of cardiomyocytes caused by hypoxia and reoxygenation via regulating IL1R2.Genes & genomics · 2020Article
- Downregulation of lncRNA ZFAS1 protects H9c2 cardiomyocytes from ischemia/reperfusion‑induced apoptosis via the miR‑590‑3p/NF‑κB signaling pathway.Molecular medicine reports · 2020Article
- PLCE1 promotes myocardial ischemia-reperfusion injury in H/R H9c2 cells and I/R rats by promoting inflammation.Bioscience reports · 2019Article
- Deletion of NFKB1 enhances canonical NF-κB signaling and increases macrophage and myofibroblast content during tendon healing.Scientific reports · 2019Article
- Diosgenin Protects Rats from Myocardial Inflammatory Injury Induced by Ischemia-Reperfusion.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Targeting TRAF3IP2 by Genetic and Interventional Approaches Inhibits Ischemia/Reperfusion-induced Myocardial Injury and Adverse Remodeling.The Journal of biological chemistry · 2017Article
- Brazilin exerts protective effects against renal ischemia-reperfusion injury by inhibiting the NF-κB signaling pathway.International journal of molecular medicine · 2016Article
- The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis.Circulation research · 2016Review
- Gypenoside Protects Cardiomyocytes against Ischemia-Reperfusion Injury via the Inhibition of Mitogen-Activated Protein Kinase Mediated Nuclear Factor Kappa B Pathway In Vitro and In Vivo.Frontiers in pharmacology · 2016Article
- Reducing effect of IL-32α in the development of stroke through blocking of NF-κB, but enhancement of STAT3 pathways.Molecular neurobiology · 2015Article
- Exercise preconditioning attenuates pressure overload-induced pathological cardiac hypertrophy.International journal of clinical and experimental pathology · 2015Article
- 5-Lipoxygenase facilitates healing after myocardial infarction.Basic research in cardiology · 2013Article
- Anti-inflammatory effect of protocatechuic aldehyde on myocardial ischemia/reperfusion injury in vivo and in vitro.Inflammation · 2013Article
- Exogenous administration of a recombinant variant of TWEAK impairs healing after myocardial infarction by aggravation of inflammation.PloS one · 2013Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nuclear factor kappaB (NF-kappaB) is a ubiquitous transcription factor activated by various stimuli implicated in ischemia-reperfusion injury. However, the role of NF-kappaB in cardiac ischemia-reperfusion injury has not yet been well defined. Therefore, we investigated reperfusion damage in mice with targeted deletion of the NF-kappaB subunit p50. Electrophoretic mobility shift assays validated NF-kappaB activation in wild-type (WT) but not p50 knockout (KO) mice. KO and WT animals underwent 30 minutes of coronary artery ligation and 24 hours of reperfusion in vivo. Ischemia-reperfusion damage was significantly reduced in the p50 KO when compared with matching WT mice. Although adhesion molecules such as intercellular adhesion molecule were up-regulated in left ventricles of p50 KO animals, fewer neutrophils infiltrated the infarct area, suggesting leukocytes as a potential mediator of the protection observed in the p50 KO. This was confirmed in adoptive transfer experiments: whereas transplantation of KO bone marrow in KO animals sustained the protective effect on ischemia-reperfusion injury, transplantation of WT bone marrow in KO animals abolished it. Thus, deletion of the NF-kappaB subunit p50 reduces ischemia-reperfusion injury in vivo, associated with less neutrophil infiltration. Bone marrow transplantation experiments indicate that impaired NF-kappaB activation in p50 KO leukocytes attenuates cardiac damage.
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