Hypertension pulmonaire : de la physiopathologie moléculaire aux anomalies hémodynamiques

Duong‐Quy, Sy; Rivière, Sophie; Bei, Yihua; Duong-Ngo, C.; Le-Dong, Nhât-Nam; Hua-Huy, T.; Dinh-Xuan, Anh Tuan

doi:10.1016/j.rmr.2012.03.009

Cited by 5 publications

(3 citation statements)

References 143 publications

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“…Hypoxic pulmonary vasoconstriction and remodeling are two vital factors for the development of HPH. 5 All hypoxia pathways result in an altered vascular endothelium and smooth muscle function. Hypoxia-induced pulmonary inflammation is the key in the early stage of the occurrence of HPH.…”

Section: Introductionmentioning

confidence: 99%

Protective effects of astragaloside IV against hypoxic pulmonary hypertension

Zhang

Chen

et al. 2018

Med. Chem. Commun.

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Section: Introductionmentioning

confidence: 99%

Protective effects of astragaloside IV against hypoxic pulmonary hypertension

Zhang

Chen

et al. 2018

Med. Chem. Commun.

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“…HPH has been recognized as the most common complication of some pulmonary diseases characterized by the vasoconstriction and remodeling of the pulmonary vascular artery which has been confirmed to play a role in the development of HPH (21,22). Exposure to a hypoxic environment for 4 weeks can be used to successfully establish a model of chronic HPH (23).…”

Section: Discussionmentioning

confidence: 99%

Effects of baicalin on collagen Ι and collagen ΙΙΙ expression in pulmonary arteries of rats with hypoxic pulmonary hypertension

Yan

Chen

et al. 2015

International Journal of Molecular Medicine

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The synthesis and accumulation of collagen play an important role in the formation and progression of hypoxic pulmonary hypertension. Baicalin has been reported to prevent bleomycin-induced pulmonary fibrosis. However, the role of baicalin in the treatment of pulmonary hypertension remains unknown. A disintegrin and metalloprotease with thrombospondin type-1 motif (ADAMTS-1) is a secreted enzyme that acts on a wide variety of extracellular matrix (ECM) substrates associated with vascular diseases. In this study, we aimed to investigate the effects of baicalin on the synthesis of collagen I in rats with pulmonary hypertension induced by hypoxia and the changes in ADAMTS-1 expression. A total of 24 Sprague Dawley rats were randomly assigned to 3 groups as follows: the control group (C), the hypoxia group (H) and the hypoxia + baicalin group (B). The rats in groups H and B were kept in a normobaric hypoxic chamber for 4 weeks, and the rats in group C were exposed to room air. We measured the hemodynamic indexes, including mean pulmonary artery pressure (mPAP), mean systemic (carotid) artery pressure (mSAP), and then calculated the mass ratio of right ventricle to left ventricle plus septum [RV/(LV + S)] to reflect the extent of right ventricular hypertrophy. We measured the mRNA and protein expression levels of type I collagen, type III collagen and ADAMTS-1 by hybridization in situ, and immunohistochemistry and western blot analysis, respectively. The results revealed that treatment with baicalin significantly reduced pulmonary artery pressure and attenuated the remodeling of the pulmonary artery under hypoxic conditions by increasing the expression of ADAMTS-1, so that the synthesis of type I collagen and its mRNA expression were inhibited. In conclusion, baicalin effectively inhibits the synthesis of collagen I in pulmonary arteries and this is associated with an increase in the expression of ADAMTS-1. Thus, treatment with baicalin may be an effective method for lowering pulmonary artery pressure and preventing pulmonary artery remodeling.

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“…In human, pulmonary circulation is the only circulation being capable of reacting by vasoconstriction with hypoxia characterized by a decline of PaO 2 less than 60 mmHg [4]. Hypoxic vasoconstriction allows to adjust pulmonary capillary perfusion to alveolar ventilation by ensuring a ventilation/perfusion ratio closer to the optimal value [5].…”

Section: Characteristics Of Pulmonary Circulationmentioning

confidence: 99%

Physiopathology of Pulmonary Hypertension: from Bio-Molecular Mechanism to Target Treatment

Duong‐Quy¹

2016

Vasc Med Surg

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Although the diagnosis and treatment of pulmonary hypertension (PH) is developed constantly in the last decade, PH remains an incurable and difficult to treat disease due to its high life disability and dreadful survival rate. The disease is characterized by sustained vasoconstriction, progressive vascular remodeling, and irreversible right heart dysfunction.The advanced knowledge in physiopathology and classification of PH in recent years is a useful tool helping physicians to improve the choice of target treatment. In addition, the remarkable progresses in understanding the molecular and cellular mechanisms of PH allow to develop new treatments. Actually, new therapeutic molecules have been discovered and their mechanisms of action are better understood and some are in preclinical and clinical trials. Preliminary results of these molecules with benefit effects on pulmonary arterial pressure and systemic hemodynamic gives a new hope for the future.

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Hypertension pulmonaire : de la physiopathologie moléculaire aux anomalies hémodynamiques

Cited by 5 publications

References 143 publications

Protective effects of astragaloside IV against hypoxic pulmonary hypertension

Protective effects of astragaloside IV against hypoxic pulmonary hypertension

Effects of baicalin on collagen Ι and collagen ΙΙΙ expression in pulmonary arteries of rats with hypoxic pulmonary hypertension

Physiopathology of Pulmonary Hypertension: from Bio-Molecular Mechanism to Target Treatment

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