Abstract
Advanced pulmonary arterial hypertension is characterized by extensive vascular remodeling that is usually resistant to vasodilator therapy. As the major component of the vascular media, decreased apoptosis of pulmonary arterial smooth muscle cell (PASMC) plays key roles during pulmonary vascular remodeling. Recent studies showed that enhancement of apoptosis of PASMC can reverse pulmonary vascular remodeling and severe pulmonary arterial hypertension. Enhancement of apoptosis of PASMC is becoming a novel strategy to reverse severe pulmonary arterial hypertension. This review analyzes some potential strategies to reverse pulmonary vascular remodeling.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Apoptosis / drug effects*
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Cell Proliferation / drug effects
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Dichloroacetic Acid / therapeutic use
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Humans
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Hypertension, Pulmonary / drug therapy*
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Hypertension, Pulmonary / physiopathology
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Lung / blood supply
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Lung / physiopathology
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Mice
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Muscle, Smooth, Vascular / drug effects*
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Muscle, Smooth, Vascular / physiopathology
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Pancreatic Elastase / antagonists & inhibitors
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Potassium Channels / analysis
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Proto-Oncogene Proteins c-bcl-2 / analysis
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Pulmonary Artery / drug effects*
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Pulmonary Artery / physiopathology
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Rats
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Vasodilator Agents / pharmacology
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rho-Associated Kinases / antagonists & inhibitors
Substances
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Potassium Channels
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Proto-Oncogene Proteins c-bcl-2
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Vasodilator Agents
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Dichloroacetic Acid
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rho-Associated Kinases
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Pancreatic Elastase