ArticleOxidative medicine and cellular longevity2013
Acute hyperglycemia abolishes ischemic preconditioning by inhibiting Akt phosphorylation: normalizing blood glucose before ischemia restores ischemic preconditioning.
Article in Oxidative medicine and cellular longevity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Fasting blood glucose-to-glycated hemoglobin ratio and functional outcomes in patients with ischemic stroke following endovascular treatment-a meta-analysis.Frontiers in neurology · 2025Pooled it
- Translational Barriers and Optimization Strategies for Remote Ischemic Conditioning to Enhance Stroke Cerebroprotection.Biomolecules · 2026Review
- Prognostic significance of stress hyperglycemia ratio in patients with type 2 diabetes mellitus and acute coronary syndromes.Thrombosis journal · 2025Article
- Acute Hyperglycemia-Induced Injury in Myocardial Infarction.International journal of molecular sciences · 2024Review
- Selective protein kinase C inhibition switches time-dependent glucose cardiotoxicity to cardioprotection.Frontiers in cardiovascular medicine · 2022Article
- Admission hyperglycemia and all-cause mortality in diabetic and non-diabetic patients with acute myocardial infarction: a tertiary center analysis.Internal and emergency medicine · 2021Article
- Influence of Hyperglycemia and Diabetes on Cardioprotection by Humoral Factors Released after Remote Ischemic Preconditioning (RIPC).International journal of molecular sciences · 2021Article
- Soluble Epoxide Hydrolase Blockade after Stroke Onset Protects Normal but Not Diabetic Mice.International journal of molecular sciences · 2021Article
- Pulsed ultrasound attenuates the hyperglycemic exacerbation of myocardial ischemia-reperfusion injury.The Journal of thoracic and cardiovascular surgery · 2021Article
- The myocardial infarct-exacerbating effect of cell-free DNA is mediated by the high-mobility group box 1-receptor for advanced glycation end products-Toll-like receptor 9 pathway.The Journal of thoracic and cardiovascular surgery · 2019Article
- Stimulation of the Beta2 Adrenergic Receptor at Reperfusion Limits Myocardial Reperfusion Injury via an Interleukin-10-Dependent Anti-Inflammatory Pathway in the Spleen.Circulation journal : official journal of the Japanese Circulation Society · 2018Article
- Neuroendocrine System Regulatory Mechanisms: Acute Coronary Syndrome and Stress Hyperglycaemia.European cardiology · 2018Review
- Remote ischemic preconditioning fails to reduce infarct size in the Zucker fatty rat model of type-2 diabetes: role of defective humoral communication.Basic research in cardiology · 2018Article
- Myocyte membrane and microdomain modifications in diabetes: determinants of ischemic tolerance and cardioprotection.Cardiovascular diabetology · 2017Review
- The spleen contributes importantly to myocardial infarct exacerbation during post-ischemic reperfusion in mice via signaling between cardiac HMGB1 and splenic RAGE.Basic research in cardiology · 2016Article
- Adenosine 2B Receptor Activation Reduces Myocardial Reperfusion Injury by Promoting Anti-Inflammatory Macrophages Differentiation via PI3K/Akt Pathway.Oxidative medicine and cellular longevity · 2015Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledThis study examined the hypothesis that acute hyperglycemia (HG) blocks ischemic preconditioning (IPC) by inhibiting Akt phosphorylation. Brief HG of approximately 400 mg/dL was induced in C57BL/6 mice via intraperitoneal injection of 20% dextrose (2 g/kg). All mice underwent 40 min LAD occlusion and 60 min reperfusion. The IPC protocol was 2 cycles of 5 min ischemia and 5 min reperfusion prior to index ischemia.
resultsIn control mice, infarct size (IF) was 51.7 ± 2.0 (% risk region). Preconditioning reduced IF by 50% to 25.8 ± 3.2 (P < 0.05 versus control). In HG mice, IF was significantly exacerbated to 58.1 ± 2.3. However, the effect of IPC completely disappeared in HG mice. Normalization of blood glucose with insulin 5 min before IPC recovered the cardioprotective effect. Administration of CCPA before index ischemia mimicked IPC effect. The cardioprotective effect of CCPA, not its chronotropic effect, completely disappeared in HG mice. Phosphorylation of cardiac tissue Akt before index ischemia was enhanced by IPC or CCPA but was significantly inhibited by HG in both groups. Normalization of glucose with insulin reversed the inhibition of Akt phosphorylation by HG.
conclusionHG abolishes the cardioprotective effect of preconditioning by inhibiting Akt phosphorylation. Normalization of blood glucose with insulin suffices to recover the cardioprotective effect of preconditioning.
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