ArticleThe Biochemical journal2000
Sustained activation of p42/p44 mitogen-activated protein kinase during recovery from simulated ischaemia mediates adaptive cytoprotection in cardiomyocytes.
Article in The Biochemical journal, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 82 citations in OpenAlex.
- SNX16 aggravates AngII-induced cardiac hypertrophy in mice via EGFR transactivation.Communications biology · 2025Article
- PEG35 as a Preconditioning Agent against Hypoxia/Reoxygenation Injury.International journal of molecular sciences · 2022Article
- Restricting mitochondrial GRK2 post-ischemia confers cardioprotection by reducing myocyte death and maintaining glucose oxidation.Science signaling · 2018Article
- Ursolic acid stimulates UCP2 expression and protects H9c2 cells from hypoxia-reoxygenation injury via p38 signaling.Journal of biosciences · 2018Article
- Loss of Protein Kinase Novel 1 (PKN1) is associated with mild systolic and diastolic contractile dysfunction, increased phospholamban Thr17 phosphorylation, and exacerbated ischaemia-reperfusion injury.Cardiovascular research · 2018Article
- Transcriptional and Post-Translational Targeting of Myocyte Stress Protein 1 (MS1) by the JNK Pathway in Cardiac Myocytes.Journal of molecular signaling · 2017Article
- Redox-dependent dimerization of p38α mitogen-activated protein kinase with mitogen-activated protein kinase kinase 3.The Journal of biological chemistry · 2017Article
- Expression and regulation of type 2A protein phosphatases and alpha4 signalling in cardiac health and hypertrophy.Basic research in cardiology · 2017Article
- Raf kinase inhibitor protein: lessons of a better way for β-adrenergic receptor activation in the heart.The Journal of physiology · 2017Review
- Aberrant developmental titin splicing and dysregulated sarcomere length in Thymosin β4 knockout mice.Journal of molecular and cellular cardiology · 2017Article
- Cardiac Fibroblast GRK2 Deletion Enhances Contractility and Remodeling Following Ischemia/Reperfusion Injury.Circulation research · 2016Article
- Protein kinase Cε-calcineurin cosignaling downstream of toll-like receptor 4 downregulates fibrosis and induces wound healing gene expression in cardiac myofibroblasts.Molecular and cellular biology · 2014Article
- HIF-1α signaling activation by post-ischemia treatment with astragaloside IV attenuates myocardial ischemia-reperfusion injury.PloS one · 2014Article
- The ERK1/2 signaling pathway is involved in sulfur dioxide preconditioning-induced protection against cardiac dysfunction in isolated perfused rat heart subjected to myocardial ischemia/reperfusion.International journal of molecular sciences · 2013Article
- Interference with ERK(Thr188) phosphorylation impairs pathological but not physiological cardiac hypertrophy.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- p42/p44-MAPK and PI3K are sufficient for IL-6 family cytokines/gp130 to signal to hypertrophy and survival in cardiomyocytes in the absence of JAK/STAT activation.Cellular signalling · 2013Article
- Article
- Post-transcriptional regulation of VEGF-A mRNA levels by mitogen-activated protein kinases (MAPKs) during metabolic stress associated with ischaemia/reperfusion.Molecular and cellular biochemistry · 2012Article
- Role of Mitogen-Activated Protein Kinases in Myocardial Ischemia-Reperfusion Injury during Heart Transplantation.Journal of transplantation · 2012Article
- A novel cardioprotective p38-MAPK/mTOR pathway.Experimental cell research · 2011Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Delayed cytoprotection (preconditioning) occurs 24 h after sublethal simulated ischaemia and reperfusion (SI/R) in neonatal rat ventricular cardiomyocytes. SI/R was used to investigate the role of activation of mitogen-activated protein kinases (MAPKs), stress-activated protein kinases (SAPKs) and phosphoinositide 3-kinase-dependent protein kinase B (PKB)/Akt in cytoprotection. SI resulted in transient dual (Thr/Tyr) phosphorylation of p42/p44-MAPK and p38-MAPK, weak phosphorylation of p46/p54-SAPK, but no phosphorylation of PKB. 'Reperfusion' caused further transient phosphorylation of p38-MAPK, but sustained phosphorylation of p42/p44-MAPK (lasting 4 h) and of Ser(473) of PKB (lasting 2 h). Furthermore, SI/R (24 h) induced delayed protection against lethal SI, as determined by an increase in cell viability ¿bioreduction of MTT [3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide]¿ and a decrease in cell injury (release of creatine kinase). Both protection and phosphorylation of p42/p44-MAPK were blocked by the MEK-1/2 (MAPK/Erk kinase-1/2) inhibitor PD98059 (50 microM) when given during SI/R, but not when given during SI alone. The p38-MAPK inhibitor SB203580 (10 microM) blocked the p38-MAPK-dependent phosphorylation of activating transcription factor 2 in vitro, and the phosphoinositide 3-kinase inhibitor wortmannin (100 nM) blocked PKB phosphorylation on Ser(473). However, neither SB203580 nor wortmannin had any effect on delayed protection. Therefore sustained activation of p42/p44-MAPK during simulated 'reperfusion' following sublethal SI mediates preconditioning in cardiomyocytes independently of transient activation of p38-MAPK or sustained activation of PKB.
Indexed as
Identifiers
10970806PMC1221324W2029808695What Socratic holds
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 Socratic graph.