Chapter title |
Altered Redox Balance in the Development of Chronic Hypoxia-induced Pulmonary Hypertension
|
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Chapter number | 7 |
Book title |
Pulmonary Vasculature Redox Signaling in Health and Disease
|
Published in |
Advances in experimental medicine and biology, January 2017
|
DOI | 10.1007/978-3-319-63245-2_7 |
Pubmed ID | |
Book ISBNs |
978-3-31-963244-5, 978-3-31-963245-2
|
Authors |
Nikki L. Jernigan, Thomas C. Resta, Laura V. Gonzalez Bosc, Jernigan, Nikki L., Resta, Thomas C., Gonzalez Bosc, Laura V. |
Abstract |
Normally, the pulmonary circulation is maintained in a low-pressure, low-resistance state with little resting tone. Pulmonary arteries are thin-walled and rely heavily on pulmonary arterial distension and recruitment for reducing pulmonary vascular resistance when cardiac output is elevated. Under pathophysiological conditions, however, active vasoconstriction and vascular remodeling lead to enhanced pulmonary vascular resistance and subsequent pulmonary hypertension (PH). Chronic hypoxia is a critical pathological factor associated with the development of PH resulting from airway obstruction (COPD, sleep apnea), diffusion impairment (interstitial lung disease), developmental lung abnormalities, or high altitude exposure (World Health Organization [WHO]; Group III). The rise in pulmonary vascular resistance increases right heart afterload causing right ventricular hypertrophy that can ultimately lead to right heart failure in patients with chronic lung disease. PH is typically characterized by diminished paracrine release of vasodilators, antimitogenic factors, and antithrombotic factors (e.g., nitric oxide and protacyclin) and enhanced production of vasoconstrictors and mitogenic factors (e.g., reactive oxygen species and endothelin-1) from the endothelium and lung parenchyma. In addition, phenotypic changes to pulmonary arterial smooth muscle cells (PASMC), including alterations in Ca(2+) homeostasis, Ca(2+) sensitivity, and activation of transcription factors are thought to play prominent roles in the development of both vasoconstrictor and arterial remodeling components of hypoxia-associated PH. These changes in PASMC function are briefly reviewed in Sect. 1 and the influence of altered reactive oxygen species homeostasis on PASMC function discussed in Sects. 2-4. |
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Mendeley readers
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Researcher | 5 | 20% |
Professor | 3 | 12% |
Student > Master | 3 | 12% |
Student > Bachelor | 2 | 8% |
Professor > Associate Professor | 2 | 8% |
Other | 3 | 12% |
Unknown | 7 | 28% |
Readers by discipline | Count | As % |
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Biochemistry, Genetics and Molecular Biology | 4 | 16% |
Medicine and Dentistry | 4 | 16% |
Nursing and Health Professions | 3 | 12% |
Pharmacology, Toxicology and Pharmaceutical Science | 1 | 4% |
Other | 1 | 4% |
Unknown | 7 | 28% |