Redox Control of Growth Factor Signaling in Heart, Lung, and Circulation
| Autor: | Kathy K. Griendling, Yuichiro J. Suzuki |
|---|---|
| Rok vydání: | 2003 |
| Předmět: |
Vascular smooth muscle
Physiology medicine.medical_treatment Clinical Biochemistry Biochemistry Muscle hypertrophy Animals Humans Medicine Growth Substances Lung Molecular Biology General Environmental Science business.industry Myocardium Growth factor Cardiac muscle Cell Biology medicine.disease Pulmonary hypertension Angiotensin II medicine.anatomical_structure Heart failure Blood Circulation Cancer research General Earth and Planetary Sciences Reactive Oxygen Species business Oxidation-Reduction Signal Transduction |
| Zdroj: | Antioxidants & Redox Signaling. 5:689-690 |
| ISSN: | 1557-7716 1523-0864 |
| Popis: | ology of the heart, lung, and circulation. In the heart, factors such as angiotensin II and endothelin-1 have been shown to induce cardiac muscle cell hypertrophy, which may result in heart failure (23). These factors, as well as others, also induce hypertrophy of the vessel wall, which may be important in the development of hypertension and atherosclerosis (2). Growth factors also play essential roles in lung diseases such as pulmonary hypertension, chronic obstructive pulmonary disease, and asthma by increasing the mass of pulmonary artery and airway smooth muscle (12, 14). At the cellular level, growth factors promote hyperplasia, hypertrophy and survival of cardiac muscle, smooth muscle, endothelial, and epithelial cells. Understanding the signal transduction mechanisms utilized by growth factors should help to identify therapeutic targets for various cardiovascular and pulmonary diseases. Regulation by reactive oxygen species (ROS) is a common element in the growth of cardiac and smooth muscle cells (18). One of the earliest demonstrations of a role for ROS in cardiovascular signaling was the observation that ROS are required for angiotensin II-mediated vascular smooth muscle cell hypertrophy (9). Since then, various growth factors have been shown to generate ROS which then serve as signaling molecules in systemic and pulmonary vascular and airway smooth muscle cells. This mechanism has been implicated in the development of systemic and pulmonary hypertension, atherosclerosis, and asthma (10, 11, 22). Furthermore, more recent experiments have provided evidence for a role of ROS in cardiac muscle cells, suggesting a role for redox regulation in the development of cardiac hypertrophy and failure (15, 20). The sources and targets of ROS have been under intense investigation. NAD(P)H oxidases appear to be promising sources of ROS during growth factor signaling (4, 10, 11). |
| Databáze: | OpenAIRE |
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