Cardioprotection from ischemia‐reperfusion injury due to Ras‐GTPase inhibition is attenuated by glibenclamide in the globally ischemic heart
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Summary
The data suggest that activation of Ras‐GTPase signaling pathways during ischemia are critical in the development of left ventricular dysfunction and that opening of mitoKATP channels, at least in part, contributes to cardioprotection produced by Ras‐ GTPase inhibition.
- Type
- article
- Published
- 2007-07-01
- Cited by
- 10
- References
- 30
- Access
- Open access
- OpenAlex
- https://openalex.org/W16850529
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:13495341
Keywords
Humanities, Political science, Philosophy
References
- Rap1A antagonizes the ability of Ras and Ras-Gap to inhibit muscarinic K+ channels.
- Antiarrhythmic effect of ischemic preconditioning during low-flow ischemia
- Contribution of Ras GTPase/MAP kinase and cytochrome P450 metabolites to deoxycorticosterone-salt-induced hypertension.
- Inhibition of Ras-GTPase, but not tyrosine kinases or Ca2+/calmodulin-dependent protein kinase II, improves recovery of cardiac function in the globally ischemic heart
- Signal transduction mechanisms involved in cardiac preconditioning: Role of Ras-GTPase, Ca2 +/calmodulin-dependent protein kinase II and epidermal growth factor receptor
- Acetylcholine, Bradykinin, Opioids, and Phenylephrine, but not Adenosine, Trigger Preconditioning by Generating Free Radicals and Opening Mitochondrial KATP Channels
- ras p21 and GAP inhibit coupling of muscarinic receptors to atrial K+ channels.
- Mitochondria and Ischemia/Reperfusion Injury
- Opposing functions of Ki- and Ha-Ras genes in the regulation of redox signals.
- Ischemic Preconditioning During Coronary Angioplast Is Prevented by Glibenclamide, a Selective ATP‐Sensitive K+ Channel Blocker
- GAP domains responsible for ras p21-dependent inhibition of muscarinic atrial K+ channel currents.
- Reactive oxygen species as mediators of signal transduction in cardiovascular disease.
- Inhibition of Ras/ERK1/2 signaling protects against postischemic renal injury.
- Preconditioning the myocardium: from cellular physiology to clinical cardiology.
- ATP-dependent potassium channels as a key target for the treatment of myocardial and vascular dysfunction
- Reactive Oxygen Species Activate p90 Ribosomal S6 Kinase via Fyn and Ras*
- Inhibition of apoptosis induced by ischemia-reperfusion prevents inflammation.
- ATP-sensitive potassium channels and myocardial preconditioning
- Differential regulation of p90 ribosomal S6 kinase and big mitogen-activated protein kinase 1 by ischemia/reperfusion and oxidative stress in perfused guinea pig hearts.
- The cell biology of acute myocardial ischemia.
Cited by
- Brief femoral artery ischaemia provides protection against myocardial ischaemia–reperfusion injury in rats: the possible mechanisms
- The effect of cardiac ischemic preconditioning on rat left ventricular gene expression profile
- Inhibition of Ras-GTPase Farnesylation and the Ubiquitin-Proteasome System or Treatment with Angiotensin-(1–7) Attenuates Spinal Cord Injury-Induced Cardiac Dysfunction
- Lipotab, a polyherbal formulation, attenuates isoprenaline-induced left ventricular remodeling and heart failure in rats
- Inhibition of Ras-GTPase signaling by FPTIII ameliorates development of cardiovascular dysfunction in diabetic-hypertensive rats.
- Ras inhibition attenuates myocardial ischemia-reperfusion injury.
- Cardioprotective Efficacy of Coriandrum sativum (L.) Seed Extract in Heart Failure Rats Through Modulation of Endothelin Receptors and Antioxidant Potential
- Molecules linked to Ras signaling as therapeutic targets in cardiac pathologies
- RASopathies and Cardiac Complications: Insights into Mechanisms, Diagnosis, and Innovative Treatments
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