Endogenous adenosine protects preconditioned heart during early minutes of reperfusion by activating Akt. - Wikidata - wikimedia - TriplyDB

Endogenous adenosine protects preconditioned heart during early minutes of reperfusion by activating Akt.

Endogenous adenosine protects preconditioned heart during early minutes of reperfusion by activating Akt.

http://www.wikidata.org/entity/Q46697064

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Therapeutic Hypothermia for Cardioprotection in Acute Myocardial Infarction Molecular mechanisms of ischemic preconditioning in the kidney Adenosine 2B Receptor Activation Reduces Myocardial Reperfusion Injury by Promoting Anti-Inflammatory Macrophages Differentiation via PI3K/Akt Pathway.Evidence for an intracellular localization of the adenosine A2B receptor in rat cardiomyocytes.AMP579 is revealed to be a potent A2b-adenosine receptor agonist in human 293 cells and rabbit hearts.Adenosine A2A receptor activation reduces infarct size in the isolated, perfused mouse heart by inhibiting resident cardiac mast cell degranulation.New insights into the regulation of inflammation by adenosine.Cardiac purinergic signalling in health and disease Ischaemic preconditioning improves proteasomal activity and increases the degradation of deltaPKC during reperfusion.A novel mitochondrial K(ATP) channel assay.Adenosine receptor-mediated cardioprotection: are all 4 subtypes required or redundant?A2B adenosine receptors protect against sepsis-induced mortality by dampening excessive inflammation.Both A2a and A2b adenosine receptors at reperfusion are necessary to reduce infarct size in mouse hearts Cardioprotective PKG-independent NO signaling at reperfusion Mitochondrial kinase signalling pathways in myocardial protection from ischaemia/reperfusion-induced necrosis.A2B adenosine receptors inhibit superoxide production from mitochondrial complex I in rabbit cardiomyocytes via a mechanism sensitive to Pertussis toxin Transgenic over expression of ectonucleotide triphosphate diphosphohydrolase-1 protects against murine myocardial ischemic injury.Extracellular Adenosine Formation by Ecto-5'-Nucleotidase (CD73) Is No Essential Trigger for Early Phase Ischemic Preconditioning G Protein-Coupled Estrogen Receptor 1 Mediates Acute Estrogen-Induced Cardioprotection via MEK/ERK/GSK-3β Pathway after Ischemia/Reperfusion.Role of Mitogen-Activated Protein Kinases in Myocardial Ischemia-Reperfusion Injury during Heart Transplantation Captopril Pretreatment Produces an Additive Cardioprotection to Isoflurane Preconditioning in Attenuating Myocardial Ischemia Reperfusion Injury in Rabbits and in Humans.Adenosine augments IL-10 production by microglial cells through an A2B adenosine receptor-mediated process All preconditioning-related G protein-coupled receptors can be demonstrated in the rabbit cardiomyocyte.Beyond anoxia: the physiology of metabolic downregulation and recovery in the anoxia-tolerant turtle.Platelet P2Y₁₂ blockers confer direct postconditioning-like protection in reperfused rabbit hearts Cardioprotection by mild hypothermia during ischemia involves preservation of ERK activity Preconditioning and postconditioning: innate cardioprotection from ischemia-reperfusion injury.Infarct limitation by a protein kinase G activator at reperfusion in rabbit hearts is dependent on sensitizing the heart to A2b agonists by protein kinase C The paradigm of postconditioning to protect the heart.Acidosis, oxygen, and interference with mitochondrial permeability transition pore formation in the early minutes of reperfusion are critical to postconditioning's success Redox signaling at reperfusion is required for protection from ischemic preconditioning but not from a direct PKC activator.Mitochondrial therapeutics for cardioprotection.Cardioprotection by ischemic postconditioning during surgical procedures.Long-acting phosphodiesterase-5 inhibitor, tadalafil, induces sustained cardioprotection against lethal ischemic injury.The Akt1 isoform is an essential mediator of ischaemic preconditioning Protein kinase C protects preconditioned rabbit hearts by increasing sensitivity of adenosine A2b-dependent signaling during early reperfusion PDE1C deficiency antagonizes pathological cardiac remodeling and dysfunction.Adenosine receptors and reperfusion injury of the heart Mechanism of cardioprotection by early ischemic preconditioning Mitochondrial reprogramming through cardiac oxygen sensors in ischaemic heart disease.

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Endogenous adenosine protects preconditioned heart during early minutes of reperfusion by activating Akt.

http://www.wikidata.org/entity/Q46697064

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2005 nî lūn-bûn

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2005年學術文章

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2005年學術文章

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Endogenous adenosine protects ...... reperfusion by activating Akt.

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Endogenous adenosine protects ...... reperfusion by activating Akt.

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American Journal of Physiology - Heart and Circulatory Physiology

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Endogenous adenosine protects ...... reperfusion by activating Akt.

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James M Downey

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Michael V Cohen

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Nataliya V Solenkova

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Viktoriya Solodushko

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P2860

Anilide derivatives of an 8-phenylxanthine carboxylic congener are highly potent and selective antagonists at human A(2B) adenosine receptors

8-Cyclopentyl-1,3-dipropylxanthine (DPCPX)--a selective high affinity antagonist radioligand for A1 adenosine receptors.

Postconditioning reduces infarct size via adenosine receptor activation by endogenous adenosine.

Amp 579 reduces contracture and limits infarction in rabbit heart by activating adenosine A2 receptors.

Myocardial protection by insulin at reperfusion requires early administration and is mediated via Akt and p70s6 kinase cell-survival signaling.

ACh and adenosine activate PI3-kinase in rabbit hearts through transactivation of receptor tyrosine kinases.

Bradykinin limits infarction when administered as an adjunct to reperfusion in mouse heart: the role of PI3K, Akt and eNOS.

CGX-1051, a peptide from Conus snail venom, attenuates infarction in rabbit hearts when administered at reperfusion.

NECA and bradykinin at reperfusion reduce infarction in rabbit hearts by signaling through PI3K, ERK, and NO.

Cross-talk between the survival kinases during early reperfusion: its contribution to ischemic preconditioning.

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