Abstract
Evidence that apoptosis plays an important role in the pathophysiology of lung diseases has been accumulated. Apoptosis signaling is classically composed of two principle pathways. One is a direct pathway from death receptor ligation to caspase cascade activation and cell death. Death receptor ligation triggers recruitment of the precursor form of caspase-8 to a death-inducing complex, through the adaptor protein FADD, which leads to caspase-8 activation. The other pathway triggered by stimuli such as drugs, radiation, infectious agents and reactive oxygen species is initiated in mitochondria. After cytochrome c is released into the cytosol from the mitochondria, it binds to Apaf1 and ATP, which then activate caspase-9. Recently, endoplasmic reticulum has also been shown to be the organelle to execute apoptosis. Further understanding of molecular mechanisms of apoptosis and its regulation by novel drugs may lead to the development of effective strategies against lung diseases. We overview the signaling pathways of apoptosis and discuss the involvement of apoptosis in the pathophysiology of various lung diseases.
Keywords: apoptosis, death receptor, mitochondria, acute lung injury, pulmonary fibrosis, bronchial asthma, pulmonary emphysema
Medicinal Chemistry
Title: Apoptosis Signaling Pathways in Lung Diseases
Volume: 1 Issue: 1
Author(s): K. Kuwano, M. Yoshimi, T. Maeyama, N. Hamada, M. Yamada and Y. Nakanishi
Affiliation:
Keywords: apoptosis, death receptor, mitochondria, acute lung injury, pulmonary fibrosis, bronchial asthma, pulmonary emphysema
Abstract: Evidence that apoptosis plays an important role in the pathophysiology of lung diseases has been accumulated. Apoptosis signaling is classically composed of two principle pathways. One is a direct pathway from death receptor ligation to caspase cascade activation and cell death. Death receptor ligation triggers recruitment of the precursor form of caspase-8 to a death-inducing complex, through the adaptor protein FADD, which leads to caspase-8 activation. The other pathway triggered by stimuli such as drugs, radiation, infectious agents and reactive oxygen species is initiated in mitochondria. After cytochrome c is released into the cytosol from the mitochondria, it binds to Apaf1 and ATP, which then activate caspase-9. Recently, endoplasmic reticulum has also been shown to be the organelle to execute apoptosis. Further understanding of molecular mechanisms of apoptosis and its regulation by novel drugs may lead to the development of effective strategies against lung diseases. We overview the signaling pathways of apoptosis and discuss the involvement of apoptosis in the pathophysiology of various lung diseases.
Export Options
About this article
Cite this article as:
Kuwano K., Yoshimi M., Maeyama T., Hamada N., Yamada M. and Nakanishi Y., Apoptosis Signaling Pathways in Lung Diseases, Medicinal Chemistry 2005; 1 (1) . https://dx.doi.org/10.2174/1573406053402497
DOI https://dx.doi.org/10.2174/1573406053402497 |
Print ISSN 1573-4064 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6638 |
- 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
Related Articles
-
Mechanisms of Neurodegeration in Type 2 Diabetes and the Neuroprotective Potential of Dipeptidyl Peptidase 4 Inhibitors
Current Medicinal Chemistry Inflammation, Endothelial Dysfunction and Arterial Stiffness as Therapeutic Targets in Cardiovascular Medicine
Current Pharmaceutical Design Pro- and Anti-Arrhythmic Effects of Anti-Inflammatory Drugs
Anti-Inflammatory & Anti-Allergy Agents in Medicinal Chemistry Patents in Targets and Drugs for Unbalanced Cytokine and Chemokine Network Mediated Disorders
Recent Patents on Inflammation & Allergy Drug Discovery α-Fibrinogenases
Current Drug Targets - Cardiovascular & Hematological Disorders Polymer Drug Conjugates: Recent Advancements in Various Diseases
Current Pharmaceutical Design There is a Link Between Erectile Dysfunction and Heart Failure: It could be Inflammation
Current Drug Targets Oxidative Stress-Induced Ischemic Heart Disease: Protection by Antioxidants
Current Medicinal Chemistry Recent Trends in the Pharmacological Activity of Isoprenyl Phenolics
Current Medicinal Chemistry Iron and Iron Chelators: A Review on Potential Effects on Skin Aging
Current Aging Science The Protective of Baicalin on Myocardial Ischemia-Reperfusion Injury
Current Pharmaceutical Biotechnology The HVJ-Envelope as an Innovative Vector System for Cardiovascular Disease
Current Gene Therapy The Role of Oxidative Stress on Necrotizing Enterocolitis in Very Low Birth Weight Infants
Current Pediatric Reviews Pathophysiogenesis of Mesial Temporal Lobe Epilepsy: Is Prevention of Damage Antiepileptogenic?
Current Medicinal Chemistry Re-Wiring the Circuit: Mitochondria as a Pharmacological Target in Liver Disease
Current Medicinal Chemistry Targeting Leukostasis for the Treatment of Early Diabetic Retinopathy
Cardiovascular & Hematological Disorders-Drug Targets TNF-α/Cycloheximide-Induced Oxidative Stress and Apoptosis in Murine Intestinal Epithelial MODE-K Cells
Current Pharmaceutical Design Diabetes-induced Epigenetic Signature in Vascular Cells
Endocrine, Metabolic & Immune Disorders - Drug Targets Editorial: Recent Advances of Cell and Gene Therapy in Kidney Diseases
Current Gene Therapy Mitochondrial Dysfunction during Sepsis
Endocrine, Metabolic & Immune Disorders - Drug Targets