ArticlePloS one2013
Isoflurane preconditioning confers cardioprotection by activation of ALDH2.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 43 citations in OpenAlex.
- Retraction: Isoflurane Preconditioning Confers Cardioprotection by Activation of ALDH2.PloS one · 2023Article
- Aldehyde Dehydrogenase 2 as a Therapeutic Target in Oxidative Stress-Related Diseases: Post-Translational Modifications Deserve More Attention.International journal of molecular sciences · 2022Review
- Longitudinal Impact of WTC Dust Inhalation on Rat Cardiac Tissue Transcriptomic Profiles.International journal of environmental research and public health · 2022Article
- Isoflurane and low-level carbon monoxide exposures increase expression of pro-survival miRNA in neonatal mouse heart.Cell stress & chaperones · 2021Article
- Longitudinal impact on rat cardiac tissue transcriptomic profiles due to acute intratracheal inhalation exposures to isoflurane.PloS one · 2021Article
- Role of aldehyde dehydrogenase 2 in ischemia reperfusion injury: An update.World journal of gastroenterology · 2018Review
- Cardioprotection induced by a brief exposure to acetaldehyde: role of aldehyde dehydrogenase 2.Cardiovascular research · 2018Article
- New and revisited approaches to preserving the reperfused myocardium.Nature reviews. Cardiology · 2017Review
- Subcellular Energetics and Metabolism: Potential Therapeutic Applications.Anesthesia and analgesia · 2017Review
- Aldehyde dehydrogenase 2 protects against oxidative stress associated with pulmonary arterial hypertension.Redox biology · 2017Article
- Human Second Window Pre-Conditioning and Post-Conditioning by Nitrite Is Influenced by a Common Polymorphism in Mitochondrial Aldehyde Dehydrogenase.JACC. Basic to translational science · 2017Article
- Article
- MicroRNA-21 Mediates Isoflurane-induced Cardioprotection against Ischemia-Reperfusion Injury via Akt/Nitric Oxide Synthase/Mitochondrial Permeability Transition Pore Pathway.Anesthesiology · 2015Article
- Article
- Isoflurane reduces hypoxia/reoxygenation-induced apoptosis and mitochondrial permeability transition in rat primary cultured cardiocytes.BMC anesthesiology · 2014Article
- Mitochondrial targets for volatile anesthetics against cardiac ischemia-reperfusion injury.Frontiers in physiology · 2014Review
- Isoflurane provides neuroprotection in neonatal hypoxic ischemic brain injury.Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2013Review
- Precision Medicine Considerations for the Management of Heart Disease and Stroke in East Asians.Cardiology plusArticle
Corrections and comments
- Retraction · 2023-09-28Concerns/Issues about Data · Concerns/Issues about Image · Duplication of/in Image · Error in Image · Original Data and/or Images not Provided and/or not Available · Unreliable Data ·
- Retracted
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The volatile anesthetic, isoflurane, protects the heart from ischemia/reperfusion (I/R) injury. Aldehyde dehydrogenase 2 (ALDH2) is thought to be an endogenous mechanism against ischemia-reperfusion injury possibly through detoxification of toxic aldehydes. We investigated whether cardioprotection by isoflurane depends on activation of ALDH2.Anesthetized rats underwent 40 min of coronary artery occlusion followed by 120 min of reperfusion and were randomly assigned to the following groups: untreated controls, isoflurane preconditioning with and without an ALDH2 inhibitor, the direct activator of ALDH2 or a protein kinase C (PKCε) inhibitor. Pretreatment with isoflurane prior to ischemia reduced LDH and CK-MB levels and infarct size, while it increased phosphorylation of ALDH2, which could be blocked by the ALDH2 inhibitor, cyanamide. Isolated neonatal cardiomyocytes were treated with hypoxia followed by reoxygenation. Hypoxia/reoxygenation (H/R) increased cardiomyocyte apoptosis and injury which were attenuated by isoflurane and forced the activation of ALDH2. In contrast, the effect of isoflurane-induced protection was almost abolished by knockdown of ALDH2. Activation of ALDH2 and cardioprotection by isoflurane were substantially blocked by the PKCε inhibitor. Activation of ALDH2 by mitochondrial PKCε plays an important role in the cardioprotection of isoflurane in myocardium I/R injury.
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Registered trials
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.