Abstract
A large amount of energy produced by active aerobic metabolism is necessary for the cochlea to maintain its function. This makes the cochlea vulnerable to blockade of cochlear blood flow and interruption of the oxygen supply. Although certain forms of human idiopathic sudden sensorineural hearing loss reportedly arise from ischemic injury, the pathological mechanism of cochlear ischemia-reperfusion injury has not been fully elucidated. Recent animal studies have shed light on the mechanisms of cochlear ischemia-reperfusion injury. It will help in the understanding of the pathology of cochlear ischemia-reperfusion injury to classify this injury into ischemic injury and reperfusion injury. Excitotoxicity, mainly observed during the ischemic period, aggravates the injury of primary auditory neurons. On the other hand, oxidative damage induced by hydroxyl radicals and nitric oxide enhances cochlear reperfusion injury. This article briefly summarizes the generation mechanisms of cochlear ischemia-reperfusion injury and potential therapeutic targets that could be developed for the effective management of this injury type.
Keywords: Cochlea, Blood flow, Ischemia-reperfusion injury, Excitotoxicity, Oxidative damage
Current Neuropharmacology
Title: Ischemia-Reperfusion Injury of the Cochlea: Pharmacological Strategies for Cochlear Protection and Implications of Glutamate and Reactive Oxygen Species
Volume: 8 Issue: 2
Author(s): Keiji Tabuchi, Bungo Nishimura, Shuho Tanaka, Kentaro Hayashi, Yuki Hirose and Akira Hara
Affiliation:
Keywords: Cochlea, Blood flow, Ischemia-reperfusion injury, Excitotoxicity, Oxidative damage
Abstract: A large amount of energy produced by active aerobic metabolism is necessary for the cochlea to maintain its function. This makes the cochlea vulnerable to blockade of cochlear blood flow and interruption of the oxygen supply. Although certain forms of human idiopathic sudden sensorineural hearing loss reportedly arise from ischemic injury, the pathological mechanism of cochlear ischemia-reperfusion injury has not been fully elucidated. Recent animal studies have shed light on the mechanisms of cochlear ischemia-reperfusion injury. It will help in the understanding of the pathology of cochlear ischemia-reperfusion injury to classify this injury into ischemic injury and reperfusion injury. Excitotoxicity, mainly observed during the ischemic period, aggravates the injury of primary auditory neurons. On the other hand, oxidative damage induced by hydroxyl radicals and nitric oxide enhances cochlear reperfusion injury. This article briefly summarizes the generation mechanisms of cochlear ischemia-reperfusion injury and potential therapeutic targets that could be developed for the effective management of this injury type.
Export Options
About this article
Cite this article as:
Tabuchi Keiji, Nishimura Bungo, Tanaka Shuho, Hayashi Kentaro, Hirose Yuki and Hara Akira, Ischemia-Reperfusion Injury of the Cochlea: Pharmacological Strategies for Cochlear Protection and Implications of Glutamate and Reactive Oxygen Species, Current Neuropharmacology 2010; 8 (2) . https://dx.doi.org/10.2174/157015910791233123
DOI https://dx.doi.org/10.2174/157015910791233123 |
Print ISSN 1570-159X |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6190 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
- Announcements
Related Articles
-
Mechanisms of Control of Neuron Survival by the Endocannabinoid System
Current Pharmaceutical Design Mitochondrial MMP Activation, Dysfunction and Arrhythmogenesis in Hyperhomocysteinemia
Current Vascular Pharmacology Human Pluripotent Stem Cells for Modelling Human Liver Diseases and Cell Therapy
Current Gene Therapy Phytochemical Therapies in Vascular Functioning: A Molecular Approach
Current Vascular Pharmacology Contribution of Stem Cells to Kidney Repair
Current Stem Cell Research & Therapy Non-Covalent Proteasome Inhibitors
Current Pharmaceutical Design Antioxidant Activities of Retinoidal Benzimidazole Or Indole Derivatives in In Vitro Model Systems
Current Medicinal Chemistry Protein-Protein Interactions in Drug Discovery
Drug Design Reviews - Online (Discontinued) Cell Therapy for Myocardial Regeneration
Current Molecular Medicine Multifunctional RNase MCPIP1 and its Role in Cardiovascular Diseases
Current Medicinal Chemistry Hydrogen Sulfide: A New Tool to Design and Develop Drugs
Clinical Anti-Inflammatory & Anti-Allergy Drugs (Discontinued) Therapeutic Applications of Crocus sativus L. (Saffron): A Review
The Natural Products Journal Metabolic Syndrome and Myocardial Infarction in Women
Current Pharmaceutical Design Cellular Mechanisms of the Protective Effect of Polyphenols on the Neurovascular Unit in Strokes
Cardiovascular & Hematological Agents in Medicinal Chemistry The Cellular Protective Effects of Rosmarinic Acid: From Bench to Bedside
Current Neurovascular Research The Response of the Aged Brain to Stroke: Too Much, Too Soon?
Current Neurovascular Research Inflammatory Reactions and Hydrocortisone in the Setting of Cardiac Surgery: An Overview
Cardiovascular & Hematological Agents in Medicinal Chemistry Neuroprotective Properties of Peroxisome Proliferator-Activated Receptor Alpha (PPARα) and its Lipid Ligands
Current Medicinal Chemistry Sex Differences in Biomarkers for Predicting Cardiovascular and Coronary Events
Current Vascular Pharmacology The Urokinase Receptor System, A Key Regulator at the Intersection between Inflammation, Immunity, and Coagulation
Current Pharmaceutical Design