Abstract
This review is focused on the mechanistic aspects of the insulin-induced H2O2 signalling pathway in neurons and the molecules affecting it, which act as risk factors for developing central insulin resistance. Insulin-induced H2O2 promotes insulin receptor activation and the mitochondria act as the insulin-sensitive H2O2 source, providing a direct molecular link between mitochondrial dysfunction and irregular insulin receptor activation. In this view, the accumulation of dysfunctional mitochondria during chronological ageing and Alzheimer’s disease (AD) is a risk factor that may contribute to the development of dysfunctional cerebral insulin receptor signalling and insulin resistance. Due to the high significance of insulin-induced H2O2 for insulin receptor activation, oxidative stress-induced upregulation of antioxidant enzymes, e.g., in AD brains, may represent another risk factor contributing to the development of insulin resistance. As insulin-induced H2O2 signalling requires fully functional mitochondria, pharmacological strategies based on activating mitochondria biogenesis in the brain are central to the treatment of diseases associated with dysfunctional insulin receptor signalling in this organ.
Keywords: Alzheimer’s disease, brain, insulin receptor, hydrogen peroxide, mitochondria
Current Neuropharmacology
Title:H2O2 Signalling Pathway: A Possible Bridge between Insulin Receptor and Mitochondria
Volume: 10 Issue: 4
Author(s): Igor A. Pomytkin
Affiliation:
Keywords: Alzheimer’s disease, brain, insulin receptor, hydrogen peroxide, mitochondria
Abstract: This review is focused on the mechanistic aspects of the insulin-induced H2O2 signalling pathway in neurons and the molecules affecting it, which act as risk factors for developing central insulin resistance. Insulin-induced H2O2 promotes insulin receptor activation and the mitochondria act as the insulin-sensitive H2O2 source, providing a direct molecular link between mitochondrial dysfunction and irregular insulin receptor activation. In this view, the accumulation of dysfunctional mitochondria during chronological ageing and Alzheimer’s disease (AD) is a risk factor that may contribute to the development of dysfunctional cerebral insulin receptor signalling and insulin resistance. Due to the high significance of insulin-induced H2O2 for insulin receptor activation, oxidative stress-induced upregulation of antioxidant enzymes, e.g., in AD brains, may represent another risk factor contributing to the development of insulin resistance. As insulin-induced H2O2 signalling requires fully functional mitochondria, pharmacological strategies based on activating mitochondria biogenesis in the brain are central to the treatment of diseases associated with dysfunctional insulin receptor signalling in this organ.
Export Options
About this article
Cite this article as:
A. Pomytkin Igor, H2O2 Signalling Pathway: A Possible Bridge between Insulin Receptor and Mitochondria, Current Neuropharmacology 2012; 10 (4) . https://dx.doi.org/10.2174/1570159X11209040311
DOI https://dx.doi.org/10.2174/1570159X11209040311 |
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
- Forthcoming Thematic Issues
Related Articles
-
Oncolytic Herpes Simplex Virus Type 1 and Host Immune Responses
Current Cancer Drug Targets Adrenomedullin in Hypertension
Current Hypertension Reviews Novel Natural and Synthetic Ligands of the Endocannabinoid System
Current Medicinal Chemistry Possible Involvement of Programmed Cell Death Pathways in the Neuroprotective Action of Polyphenols
Current Alzheimer Research The Antimalarial Drug Pyronaridine Inhibits Topoisomerase II in Breast Cancer Cells and Hinders Tumor Progression In Vivo
Clinical Cancer Drugs A Novel µ-Opioid Receptor Ligand with High In Vitro and In Vivo Agonist Efficacy
Current Medicinal Chemistry Polyethylenimine as a Promising Vector for Targeted siRNA Delivery
Current Clinical Pharmacology Role of Generation, Architecture, pH and Ionic Strength on Successful siRNA Delivery and Transfection by Hybrid PPV-PAMAM Dendrimers
Current Medicinal Chemistry Riluzole Inhibits Proliferation, Migration and Cell Cycle Progression and Induces Apoptosis in Tumor Cells of Various Origins
Anti-Cancer Agents in Medicinal Chemistry Potential Usage of ING Family Members in Cancer Diagnostics and Molecular Therapy
Current Drug Targets Organic Modification of the Polysaccharide Alginate
Mini-Reviews in Organic Chemistry Metabolism of the Endocannabinoids Anandamide and 2-Arachidonoyl Glycerol, A Review, with Emphasis on the Pharmacology of Fatty Acid Amide Hydrolase, A Possible Target for the Treatment of Neurodegenerative Diseases and Pain
Current Medicinal Chemistry - Central Nervous System Agents Therapeutical Potential of CB<sub>2</sub> Receptors in Immune-Related Diseases
Current Molecular Pharmacology Recent Multi-target Approaches on the Development of Anti- Alzheimer's Agents Integrating Metal Chelation Activity
Current Medicinal Chemistry Anticancer Agents: VTA or VDA
Current Bioactive Compounds Non-Cholinergic Pharmacotherapy Approaches to Alzheimers Disease: The Use of Non-Steroidal Anti-Inflammatory Drugs
CNS & Neurological Disorders - Drug Targets Purines and Pyrimidines: Metabolism, Function and Potential as Therapeutic Options in Neurodegenerative Diseases
Current Protein & Peptide Science Recent Developments in Targeted Therapies of the RAF-MEK and PI3KAKT Pathways in Cancer Treatment
Current Cancer Therapy Reviews Progress in Small Molecule Therapeutics for the Treatment of Retinoblastoma
Mini-Reviews in Medicinal Chemistry A Proteomic Analysis of Human Uterine Myoma
Current Protein & Peptide Science