ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2023
CaMKK2 alleviates myocardial ischemia/reperfusion injury by inhibiting oxidative stress and inflammation via the action on the AMPK-AKT-GSK-3β/Nrf2 signaling cascade.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 15 citations in OpenAlex.
- Sacubitril/Valsartan Ameliorates Inflammation and Oxidative Stress in Hypertensive Heart Disease by Upregulating CAMKK2 Protein and Modulating the AMPK/AKT/GSK-3β Axis.The Kaohsiung journal of medical sciences · 2026Article
- Silica Nanoparticles Induce BV-2 Cells Autophagy Via activation of NLRP3 inflammasome and CaMKK2 Signaling Pathways.Molecular neurobiology · 2026Article
- Remote ischemic preconditioning protects heart via modulation of purinergic signaling and AMPK-mediated autophagy in rat model of ischemia reperfusion injury.Iranian journal of basic medical sciences · 2026Article
- Physiological and molecular dynamic changes during 23-day high-altitude exposure reveal novel biomarkers for acclimatization.Frontiers in physiology · 2026Article
- Cardioprotective response of remote ischemic preconditioning: Revealing possible role of cannabinoid type 2 receptor and AMPK-mediated autophagy in rats.Journal of cardiovascular and thoracic research · 2025Article
- Mechanisms of Adipose Tissue Metabolism in Naturally Grazing Sheep at Different Growth Stages: Insights from mRNA and miRNA Profiles.International journal of molecular sciences · 2025Article
- Alginate oligosaccharides alleviates gestational diabetes mellitus through reducing oxidative stress and improving gut microbiota.CytoJournal · 2025Article
- Inhalation Anesthetics Play a Janus-Faced Role in Self-Renewal and Differentiation of Stem Cells.Biomolecules · 2024Review
- Artemisinin conferred cytoprotection to human retinal pigment epithelial cells exposed to amiodarone-induced oxidative insult by activating the CaMKK2/AMPK/Nrf2 pathway.Journal of translational medicine · 2024Article
- Lithium alleviates paralysis in experimental autoimmune neuritis in Lewis rats by modulating glycogen synthase kinase-3β activity.Journal of veterinary science · 2024Article
- Mitochondrial network remodeling of the diabetic heart: implications to ischemia related cardiac dysfunction.Cardiovascular diabetology · 2024Review
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Authors and funding
4 authors at 2 institutions in 1 country.
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Abstract
objectiveCalcium/calmodulin-dependent protein kinase kinase 2 (CaMKK2) can regulate numerous biological processes and is implicated in diverse pathological processes. Yet its role in myocardial ischemia/reperfusion (MI/R) injury remains unknown. This project explored the possible functions and mechanisms of CaMKK2 in MI/R injury.
methodsA rat model of MI/R in vivo was established using the left anterior descending coronary artery ligation method. Rat cardiomyocytes were exposed to hypoxia/reoxygenation (H/R) in vitro to establish a cell model. Overexpression of CaMKK2 was achieved by infecting recombinant adeno-associated virus or adenovirus expressing CaMKK2. Real-time quantitative PCR, immunoblotting, TTC staining, TUNEL assay, ELISA, oxidative stress detection assays, flow cytometry, and CCK-8 assay were carried out.
resultsA decline in CaMKK2 levels was induced by MI/R in vivo or H/R in vitro. Up-modulation of CaMKK2 in rats ameliorated the cardiac injury evoked by MI/R injury accompanied by suppression of cardiac apoptosis, oxidative stress, and proinflammatory response. Rat cardiomyocytes with CaMKK2 overexpression were also protected from H/R damage by inhibiting apoptosis, oxidative stress, and proinflammatory response. CaMKK2 overexpression led to increased phosphorylation of AMPK, AKT, and GSK-3β, and enhanced activation of Nrf2 under MI/R or H/R conditions. Inhibition of AMPK abolished CaMKK2-mediated Nrf2 activation and relevant cardioprotective effect. Restraint of Nrf2 also diminished CaMKK2-mediated relevant cardioprotective effect.
conclusionsUp-regulation of CaMKK2 provides a therapeutic benefit in the rat model of MI/R injury by boosting the Nrf2 pathway through regulation of AMPK/AKT/GSK-3β, which suggests CaMKK2 as a new molecular target for the treatment of MI/R injury.
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