ArticleAmerican journal of physiology. Heart and circulatory physiology2012
Creatine kinase overexpression improves ATP kinetics and contractile function in postischemic myocardium.
Article in American journal of physiology. Heart and circulatory physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- Hypercontractility and Oxidative Stress Drive Creatine Kinase Dysfunction in Hypertrophic Cardiomyopathy.Circulation · 2025Article
- Article
- Extracellular vesicles from human cardiac stromal cells up-regulate cardiomyocyte protective responses to hypoxia.Stem cell research & therapy · 2024Article
- Maintaining energy provision in the heart: the creatine kinase system in ischaemia-reperfusion injury and chronic heart failure.Clinical science (London, England : 1979) · 2024Review
- Identification of potential biomarkers for cerebral palsy and the development of prediction models.Experimental biology and medicine (Maywood, N.J.) · 2024Article
- CardiacHeart failure reviews · 2023Review
- Synergistic effect on cardiac energetics by targeting the creatine kinase system: in vivo application of high-resolutionJournal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance · 2023Article
- Ontogeny of cardiomyocytes: ultrastructure optimization to meet the demand for tight communication in excitation-contraction coupling and energy transfer.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Review
- Quantification of creatine kinase reaction rate in mouse hindlimb using phosphorus-31 magnetic resonance spectroscopic fingerprinting.NMR in biomedicine · 2021Article
- Proteomic Analysis of Uterine Tissues During Peri-Implantation Period in Mice with Experimentally Induced Adenomyosis that Treated with anti-Ngf: Implications for Cell-Cell Adhesion and Metabolic Processes.Reproductive sciences (Thousand Oaks, Calif.) · 2021Article
- The Pitfalls ofFrontiers in physiology · 2021Review
- Protein target identification of ginsenosides in skeletal muscle tissues: discovery of natural small-molecule activators of muscle-type creatine kinase.Journal of ginseng research · 2020Article
- Energetic Interactions Between Subcellular Organelles in Striated Muscles.Frontiers in cell and developmental biology · 2020Review
- The creatine kinase system as a therapeutic target for myocardial ischaemia-reperfusion injury.Biochemical Society transactions · 2018Review
- Over-expression of mitochondrial creatine kinase in the murine heart improves functional recovery and protects against injury following ischaemia-reperfusion.Cardiovascular research · 2018Article
- A comprehensive review of the bioenergetics of fatty acid and glucose metabolism in the healthy and failing heart in nondiabetic condition.Heart failure reviews · 2017Review
- Increasing creatine kinase activity protects against hypoxia / reoxygenation injury but not against anthracycline toxicity in vitro.PloS one · 2017Article
- Article
- A link between ATP and SUR2A: A novel mechanism explaining cardioprotection at high altitude.International journal of cardiology · 2015Review
- Modular organization of cardiac energy metabolism: energy conversion, transfer and feedback regulation.Acta physiologica (Oxford, England) · 2015Review
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Reduced myofibrillar ATP availability during prolonged myocardial ischemia may limit post-ischemic mechanical function. Because creatine kinase (CK) is the prime energy reserve reaction of the heart and because it has been difficult to augment ATP synthesis during and after ischemia, we used mice that overexpress the myofibrillar isoform of creatine kinase (CKM) in cardiac-specific, conditional fashion to test the hypothesis that CKM overexpression increases ATP delivery in ischemic-reperfused hearts and improves functional recovery. Isolated, retrograde-perfused hearts from control and CKM mice were subjected to 25 min of global, no-flow ischemia and 40 min of reperfusion while cardiac function [rate pressure product (RPP)] was monitored. A combination of (31)P-nuclear magnetic resonance experiments at 11.7T and biochemical assays was used to measure the myocardial rate of ATP synthesis via CK (CK flux) and intracellular pH (pH(i)). Baseline CK flux was severalfold higher in CKM hearts (8.1 ± 1.0 vs. 32.9 ± 3.8, mM/s, control vs. CKM; P < 0.001) with no differences in phosphocreatine concentration [PCr] and RPP. End-ischemic pH(i) was higher in CKM hearts than in control hearts (6.04 ± 0.12 vs. 6.37 ± 0.04, control vs. CKM; P < 0.05) with no differences in [PCr] and [ATP] between the two groups. Post-ischemic PCr (66.2 ± 1.3 vs. 99.1 ± 8.0, %preischemic levels; P < 0.01), CK flux (3.2 ± 0.4 vs. 14.0 ± 1.2 mM/s; P < 0.001) and functional recovery (13.7 ± 3.4 vs. 64.9 ± 13.2%preischemic RPP; P < 0.01) were significantly higher and lactate dehydrogenase release was lower in CKM than in control hearts. Thus augmenting cardiac CKM expression attenuates ischemic acidosis, reduces injury, and improves not only high-energy phosphate content and the rate of CK ATP synthesis in postischemic myocardium but also recovery of contractile function.
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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 OpenQuestion graph.