Abstract
Carbon monoxide (CO) is an invisible, chemically inert, colorless and odorless gas and is toxic at high concentrations due to its interference with oxygen delivery. However, CO is endogenously and physiologically generated in mammalian cells via the catabolism of heme in a rate-limiting step of heme oxygenase systems, and CO potently protects against cellular injury. CO relaxes blood vessels and exerts anti-thrombotic effects by inhibiting platelet aggregation and derepressing fibrinolysis. In addition, CO reduces ischemia/reperfusion injury and inflammatory responses. CO inhibits apoptosis of endothelial and epithelial cells and reduces proliferation of smooth muscle cells, fibroblasts and T lymphocytes. Thus, there is accumulating evidence to support the notion that CO treatment of transplant donors, organs, or recipients can prevent graft dysfunction due to rejection or ischemia/reperfusion injury. This invited review discusses recent advances and current knowledge pertaining to CO research in the field of transplantation. In addition, we will discuss the clinical applicability of CO as a promising therapeutic strategy for the treatment of transplant patients.
Keywords: Carbon monoxide, transplantation, ischemia reperfusion, rejection
Current Pharmaceutical Biotechnology
Title:Application of Carbon Monoxide for Transplantation
Volume: 13 Issue: 6
Author(s): Atsunori Nakao and Yoshiya Toyoda
Affiliation:
Keywords: Carbon monoxide, transplantation, ischemia reperfusion, rejection
Abstract: Carbon monoxide (CO) is an invisible, chemically inert, colorless and odorless gas and is toxic at high concentrations due to its interference with oxygen delivery. However, CO is endogenously and physiologically generated in mammalian cells via the catabolism of heme in a rate-limiting step of heme oxygenase systems, and CO potently protects against cellular injury. CO relaxes blood vessels and exerts anti-thrombotic effects by inhibiting platelet aggregation and derepressing fibrinolysis. In addition, CO reduces ischemia/reperfusion injury and inflammatory responses. CO inhibits apoptosis of endothelial and epithelial cells and reduces proliferation of smooth muscle cells, fibroblasts and T lymphocytes. Thus, there is accumulating evidence to support the notion that CO treatment of transplant donors, organs, or recipients can prevent graft dysfunction due to rejection or ischemia/reperfusion injury. This invited review discusses recent advances and current knowledge pertaining to CO research in the field of transplantation. In addition, we will discuss the clinical applicability of CO as a promising therapeutic strategy for the treatment of transplant patients.
Export Options
About this article
Cite this article as:
Nakao Atsunori and Toyoda Yoshiya, Application of Carbon Monoxide for Transplantation, Current Pharmaceutical Biotechnology 2012; 13 (6) . https://dx.doi.org/10.2174/138920112800399266
DOI https://dx.doi.org/10.2174/138920112800399266 |
Print ISSN 1389-2010 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4316 |

- Author Guidelines
- Bentham Author Support Services (BASS)
- 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
Related Articles
-
Heme Arginate Pretreatment Attenuates Pulmonary NF-κB and AP-1 Activation Induced by Hemorrhagic Shock via Heme Oxygenase-1 Induction
Medicinal Chemistry Minocycline and Doxycycline: More Than Antibiotics
Current Molecular Pharmacology Relationship Between the Pharmacokinetics of Levosimendan and Its Effects on Cardiovascular System
Current Drug Metabolism Mild Systemic Inflammation has a Neuroprotective Effect After Stroke in Rats
Current Neurovascular Research Interaction of Carbon Monoxide with Transition Metals: Evolutionary Insights into Drug Target Discovery
Current Drug Targets Classical Inhibitors of NOX NAD(P)H Oxidases Are Not Specific
Current Drug Metabolism PDE5 Inhibitor Treatment Options for Urologic and Non-Urologic Indications: 2012 Update
Current Pharmaceutical Design Inhibition of Inflammation by a p38 MAP Kinase Targeted Cell Permeable Peptide
Medicinal Chemistry Viral Anti-Inflammatory Reagents: The Potential for Treatment of Arthritic and Vasculitic Disorders
Endocrine, Metabolic & Immune Disorders - Drug Targets The Effects of Obesity on the Cerebral Vasculature
Current Vascular Pharmacology Efficient Expression and Purification of Recombinant Therapeutic Protein Candidates, Human Midkine and Pleiotrophin
Current Pharmaceutical Biotechnology Mitochondria as an Easy Target to Oxidative Stress Events in Parkinson's Disease
CNS & Neurological Disorders - Drug Targets From Bone Marrow to Cardiac Atrial Appendage Stem Cells for Cardiac Repair: A Review
Current Medicinal Chemistry Hypertension in Children After Renal Transplantation
Current Hypertension Reviews The Atherosclerosis Time-Line and the Role of the Endothelium
Current Medicinal Chemistry - Immunology, Endocrine & Metabolic Agents TNF-α Inhibitors with Anti-Oxidative Stress Activity from Natural Products
Current Topics in Medicinal Chemistry Recent Advances on the Antiatherogenic Effects of HDL-Derived Proteins and Mimetic Peptides
Current Pharmaceutical Design Review of the Biological Activity of Maslinic Acid
Current Drug Targets The Role of Blood-Brain Barrier Transporters in Pathophysiology and Pharmacotherapy of Stroke
Current Pharmaceutical Design Integrin Function and Signaling as Pharmacological Targets in Cardiovascular Diseases and in Cancer
Current Pharmaceutical Design