ArticleAmerican journal of physiology. Heart and circulatory physiology2013
Kir6.2 is not the mitochondrial KATP channel but is required for cardioprotection by ischemic preconditioning.
Article in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 43 citations in OpenAlex.
- Intracellular Calcium Changes Correlate with Mitochondrial Dynamics After Differential Modulation of KATP Channels in a Cellular Model of Parkinson's Disease.Neurochemical research · 2025Article
- A New Potassium Channel on the Endoplasmic Reticulum Membrane in a Rat Brain: Electropharmacology and Molecular Evidence.Basic and clinical neuroscience · 2025Article
- Exploring the Pathophysiology of ATP-Dependent Potassium Channels in Insulin Resistance.International journal of molecular sciences · 2024Review
- KArhiv za farmaciju · 2024Article
- Article
- Routes for Potassium Ions across Mitochondrial Membranes: A Biophysical Point of View with Special Focus on the ATP-Sensitive KBiomolecules · 2021Review
- Review
- Kir6.1 improves cardiac dysfunction in diabetic cardiomyopathy via the AKT-FoxO1 signalling pathway.Journal of cellular and molecular medicine · 2021Article
- Novel cholesterol-dependent regulation of cardiac KPhysiological reports · 2021Article
- Diazoxide affects mitochondrial bioenergetics by the opening of mKATP channel on submicromolar scale.BMC molecular and cell biology · 2020Article
- Single-Channel Properties of the ROMK-Pore-Forming Subunit of the Mitochondrial ATP-Sensitive Potassium Channel.International journal of molecular sciences · 2019Article
- Article
- Functional protection against cardiac diseases depends on ATP-sensitive potassium channels.Journal of cellular and molecular medicine · 2018Review
- The Slo(w) path to identifying the mitochondrial channels responsible for ischemic protection.The Biochemical journal · 2017Review
- Plasticity of sarcolemmal KATP channel surface expression: relevance during ischemia and ischemic preconditioning.American journal of physiology. Heart and circulatory physiology · 2016Article
- Cardiac Slo2.1 Is Required for Volatile Anesthetic Stimulation of K+ Transport and Anesthetic Preconditioning.Anesthesiology · 2016Article
- Cardiovascular KPathobiology of aging & age related diseases · 2016Review
- KATP Channels in the Cardiovascular System.Physiological reviews · 2016Review
- Reconciling the IPC and Two-Hit Models: Dissecting the Underlying Cellular and Molecular Mechanisms of Two Seemingly Opposing Frameworks.Journal of immunology research · 2015Review
- Cardiac ion channels.Channels (Austin, Tex.) · 2015Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
ATP-sensitive K(+) (KATP) channels that contain K(+) inward rectifier subunits of the 6.2 isotype (Kir6.2) are important regulators of the cardiac response to ischemia-reperfusion (I/R) injury. Opening of these channels is implicated in the cardioprotective mechanism of ischemic preconditioning (IPC), but debate surrounds the contribution of surface KATP (sKATP) versus mitochondrial KATP (mKATP) channels. While responses to I/R injury and IPC have been examined in Kir6.2(-/-) mice before, breeding methods and other technical obstacles may have confounded interpretations. The aim of this study was to elucidate the role of Kir6.2 in cardioprotection and mKATP activity, using conventionally bred Kir6.2(-/-) mice with wild-type littermates as controls. We found that perfused hearts from Kir6.2(-/-) mice exhibited a normal baseline response to I/R injury, were not protected by IPC, and showed a blunted response to the IPC mimetic drug diazoxide. These data suggest that the loss of IPC in Kir6.2(-/-) hearts is not due to an underlying difference in I/R sensitivity. Furthermore, mKATP channel activity was identical in cardiac mitochondria isolated from wild-type versus Kir6.2(-/-) mice, suggesting no role for Kir6.2 in the mKATP. Collectively, these data indicate that Kir6.2 is required for the full response to IPC or diazoxide but is not involved in mKATP formation.
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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.