Abstract
The intent of this article is to summarize current body of knowledge on the potential implication of the xanthine oxidase pathway (XO) on skeletal muscle damage. The possible involvement of the XO pathway in muscle damage is exemplified by the role of XO inhibitors (e.g., allopurinol) in attenuating muscle damage. Reliance on this pathway (as well as on the purine nucleotide cycle) could be exacerbated in conditions of low muscle glycogen availability. Thus, we also summarize current hypotheses on the etiology of both baseline and exertional muscle damage in McArdle disease, a condition caused by inherited deficiency of myophosphorylase. Because myophosphorylase catalyzes the first step of muscle glycogen breakdown, patients are unable to obtain energy from their muscle glycogen stores. Finally, we provide preliminary data from our laboratory on the potential implication of the XO pathway in the muscle damage that is commonly experienced by these patients.
Keywords: McArdle disease, xanthine oxidase, muscle damage, rhabdomyolysis, oxidative stress.
Current Pharmaceutical Design
Title:Xanthine Oxidase Pathway and Muscle Damage. Insights from McArdle Disease
Volume: 22 Issue: 18
Author(s): Helios Pareja-Galeano, Alejandro Santos-Lozano, María Morán, Fabian Sanchis-Gomar, Rafael Alis, Alfredo Santalla, Alejandro F. San Juan, Jorge Díez-Bermejo, Miguel A. Martín, Joaquín Arenas and Alejandro Lucia
Affiliation:
Keywords: McArdle disease, xanthine oxidase, muscle damage, rhabdomyolysis, oxidative stress.
Abstract: The intent of this article is to summarize current body of knowledge on the potential implication of the xanthine oxidase pathway (XO) on skeletal muscle damage. The possible involvement of the XO pathway in muscle damage is exemplified by the role of XO inhibitors (e.g., allopurinol) in attenuating muscle damage. Reliance on this pathway (as well as on the purine nucleotide cycle) could be exacerbated in conditions of low muscle glycogen availability. Thus, we also summarize current hypotheses on the etiology of both baseline and exertional muscle damage in McArdle disease, a condition caused by inherited deficiency of myophosphorylase. Because myophosphorylase catalyzes the first step of muscle glycogen breakdown, patients are unable to obtain energy from their muscle glycogen stores. Finally, we provide preliminary data from our laboratory on the potential implication of the XO pathway in the muscle damage that is commonly experienced by these patients.
Export Options
About this article
Cite this article as:
Pareja-Galeano Helios, Santos-Lozano Alejandro, Morán María, Sanchis-Gomar Fabian, Alis Rafael, Santalla Alfredo, F. San Juan Alejandro, Díez-Bermejo Jorge, A. Martín Miguel, Arenas Joaquín and Lucia Alejandro, Xanthine Oxidase Pathway and Muscle Damage. Insights from McArdle Disease, Current Pharmaceutical Design 2016; 22 (18) . https://dx.doi.org/10.2174/1381612822666160210144419
DOI https://dx.doi.org/10.2174/1381612822666160210144419 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
- 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
-
A Rapid and Simple UPLC Method for the Quantitative Determination of Compound X22 in Rat Plasma and its Application to a Pharmacokinetic Study
Current Pharmaceutical Analysis Role of Oxidative-Nitrosative Stress and Downstream Pathways in Various Forms of Cardiomyopathy and Heart Failure
Current Vascular Pharmacology Vehicles for Lipophilic Drugs: Implications for Experimental Design, Neuroprotection, and Drug Discovery
Current Neurovascular Research Good, Bad, Mobile Elements: Genome’s Most Successful “Parasites” as Emerging Players in Cell and Organismal Aging
Current Pharmaceutical Design Dissecting the Biological Effects of Isoflurane through the Mechanistic Target of Rapamycin (mTOR) and microRNAs (miRNAs)
Current Neurovascular Research Cyclooxygenase-2 Inhibitors as a Therapeutic Target in Inflammatory Diseases
Current Medicinal Chemistry Nitric Oxide as a Marker for Levo-Thyroxine Therapy in Subclinical Hypothyroid Patients
Current Vascular Pharmacology Clinical Evidence of Intravitreal Triamcinolone Acetonide in the Management of Age-Related Macular Degeneration
Current Drug Targets Skeletal Myoblasts for Heart Regeneration and Repair: State of the Art and Perspectives on the Mechanisms for Functional Cardiac Benefits
Current Pharmaceutical Design Monitoring Cell Therapy Using Iron Oxide MR Contrast Agents
Current Pharmaceutical Biotechnology Oxidative Stress and Mitochondrial Dysfunction in Sepsis: A Potential Therapy with Mitochondria-Targeted Antioxidants
Infectious Disorders - Drug Targets Hematopoietic Progenitor and Stem Cells Circulate by Surfing on Intracellular Ca2+ Waves: A Novel Target for Cell-based Therapy and Anti-cancer Treatment?
Current Signal Transduction Therapy Selection of Potential Pharmacological Targets in ALS Based on Whole- Genome Expression Profiling
Current Medicinal Chemistry The Role of the Chemokines in Myocardial Ischemia and Reperfusion
Current Vascular Pharmacology Crystal Structure of a Cu,Zn Superoxide Dismutase From the Thermophilic Fungus <i>Chaetomium thermophilum</i>
Protein & Peptide Letters Inflammation in Coronary Artery Disease and Acute Myocardial Infarction - is the Stage Set for Novel Therapies?
Current Pharmaceutical Design Oxidative Stress Upregulates PDCD4 Expression in Patients with Gastric Cancer via miR-21
Current Pharmaceutical Design Editorial [Pharmacology and Therapeutic Activity of Purinergic Drugs for Disorders of the Nervous System]
CNS & Neurological Disorders - Drug Targets Colloidal Supramolecular Aggregates for Therapeutic Application in Neuromedicine
Current Medicinal Chemistry Neurotrophic Factors in Combination: A Possible new Therapeutic Strategy to Influence Pathophysiology of Spinal Cord Injury and Repair Mechanisms
Current Pharmaceutical Design