Key result
Impaired synthesis or release of endothelium-derived relaxing factors and increased contracting factors induce persistent vascular contraction and pulmonary artery remodeling, driving the progression of pulmonary arterial hypertension.
Why the study?
Impaired synthesis or release of EDRFs induces persistent vascular contraction and remodeling leading to PAH, prompting a summary of how EDRFs and EDCFs affect pulmonary vascular homeostasis and novel mechanisms of endothelial dysfunction.
Answers are grounded in this paper and cite their sources.
Endothelial dysfunction driven by an imbalance between endothelium-derived relaxing and contracting factors is a critical pathogenic mechanism in the development and progression of pulmonary arterial hypertension.
Pulmonary arterial hypertension (PAH) is a progressive and fatal disease. Sustained pulmonary vasoconstriction and concentric pulmonary vascular remodeling contribute to the elevated pulmonary vascular resistance and pulmonary artery pressure in PAH. Endothelial cells regulate vascular tension by producing endothelium-derived relaxing factors (EDRFs) and endothelium-derived contracting factors (EDCFs). Homeostasis of EDRF and EDCF production has been identified as a marker of the endothelium integrity. Impaired synthesis or release of EDRFs induces persistent vascular contraction and pulmonary artery remodeling, which subsequently leads to the development and progression of PAH. In this review, the authors summarize how EDRFs and EDCFs affect pulmonary vascular homeostasis, with special attention to the recently published novel mechanisms related to endothelial dysfunction in PAH and drugs associated with EDRFs and EDCFs.
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Zhu et al. (2022) conducted a review in Pulmonary Arterial Hypertension. Endothelium-derived relaxing and contracting factors was evaluated. Impaired synthesis or release of endothelium-derived relaxing factors and increased contracting factors induce persistent vascular contraction and pulmonary artery remodeling, driving the progression of pulmonary arterial hypertension.
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