Drag-reducing polymers attenuates pulmonary vascular remodeling and right ventricular dysfunction in a rat model of chronic hypoxia-induced pulmonary hypertension

Wang, Yali; Feng, Weiwei; Feng, Huijuan; Wu, Yunjiang; Zhou, Jun; Xu, Yan; Shao, Xiaoliang; Hu, Tao

doi:10.3233/ch-190668

Cited by 4 publications

(4 citation statements)

References 31 publications

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“…On the other hand, a recent study in rats exposed to hypobaric hypoxia (10% O 2 ) administered soluble macromolecules termed drag-reducing polymers and determined that these drugs attenuate right ventricular dysfunction and hypertrophy [114]. Another drug used to decrease PH-induced RVH in mice under hypobaric hypoxia (0.5 atm) is bosentan, an endothelin receptor antagonist; however, bosentan also induced a decrease in macrophages, IL-6, and MCP-1 in the lung [115].…”

Section: Pharmacological and Gene Therapymentioning

confidence: 99%

Oxidative Stress, Kinase Activity and Inflammatory Implications in Right Ventricular Hypertrophy and Heart Failure under Hypobaric Hypoxia

Peña

Brito

Alam

et al. 2020

IJMS

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High altitude (hypobaric hypoxia) triggers several mechanisms to compensate for the decrease in oxygen bioavailability. One of them is pulmonary artery vasoconstriction and its subsequent pulmonary arterial remodeling. These changes can lead to pulmonary hypertension and the development of right ventricular hypertrophy (RVH), right heart failure (RHF) and, ultimately to death. The aim of this review is to describe the most recent molecular pathways involved in the above conditions under this type of hypobaric hypoxia, including oxidative stress, inflammation, protein kinases activation and fibrosis, and the current therapeutic approaches for these conditions. This review also includes the current knowledge of long-term chronic intermittent hypobaric hypoxia. Furthermore, this review highlights the signaling pathways related to oxidative stress (Nox-derived O2.- and H2O2), protein kinase (ERK5, p38α and PKCα) activation, inflammatory molecules (IL-1β, IL-6, TNF-α and NF-kB) and hypoxia condition (HIF-1α). On the other hand, recent therapeutic approaches have focused on abolishing hypoxia-induced RVH and RHF via attenuation of oxidative stress and inflammatory (IL-1β, MCP-1, SDF-1 and CXCR-4) pathways through phytotherapy and pharmacological trials. Nevertheless, further studies are necessary.

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Section: Pharmacological and Gene Therapymentioning

confidence: 99%

Oxidative Stress, Kinase Activity and Inflammatory Implications in Right Ventricular Hypertrophy and Heart Failure under Hypobaric Hypoxia

Peña

Brito

Alam

et al. 2020

IJMS

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“…The degree of right cardiac hypertrophy was calculated and evaluated according to right ventricular hypertrophy index: (RV/[LV+S]). 19 …”

Section: Methodsmentioning

confidence: 99%

“…The hearts excised from the mice were washed with PBS and divided into two parts: right ventricle (RV) and left ventricle plus interventricular septum (LV+S), and their dry weights were weighed, respectively. The degree of right cardiac hypertrophy was calculated and evaluated according to right ventricular hypertrophy index: (RV/[LV+S]) 19 …”

Section: Methodsmentioning

confidence: 99%

Calpain‐1 mediates vascular remodelling and fibrosis via HIF‐1α in hypoxia‐induced pulmonary hypertension

Deng

Tian

Sun

et al. 2022

J Cellular Molecular Medi

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Pulmonary hypertension (PH) is a fatal vascular disease defined as pulmonary vascular resistance (PVR) > 3 wood units associated with mean pulmonary arterial pressure (mPAP) ≥20 mm Hg at rest. 1According to the most recent clinical classification of PH, Hypoxic pulmonary hypertension (HPH) belongs to the third category of this disease and characterized by pulmonary arteries remodelling, which include arterial fibrosis, hyperproliferation and abnormal apoptosis. 1,2 HPH is a vascular disease caused by continuous exposure to hypoxic environment. Chronic hypoxia can lead to abnormal contraction and remodelling of pulmonary vessels, increase pulmonary

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“…Studies have shown that right ventricular remodeling and its function are closely related to symptom severity and survival of HPH [6][7][8]. Increased cardiac afterload and right Disclaimer/Publisher's Note: The statements, opinions, and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s).…”

Section: Introductionmentioning

confidence: 99%

Hypoxia-Induced Cardiomyocyte Apoptosis Exacerbates Cardiomyocyte Hypertrophy and Myocardial Injury through p38 MAPK Pathway in SD Rats

Li¹,

Pu²,

Xu³

et al. 2023

Preprint

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Right ventricular remodeling and its function are closely related to the symptom severity and survival of hypoxia pulmonary hypertension, but molecular mechanisms of cardiomyocyte hypertrophy and myocardial injury remain unclear. It evaluated the cardiac function (by right cardiac catheterization to measure right ventricular systolic pressure and mean pulmonary artery pressure), myocardial tissue morphology（Haematoxylin and Eosin）, myocardial hypertrophy (Wheat Germ Agglutinin Staining), then RNA sequencing was applied to explore the mechanism, which results were verified by western blot in final. Hypoxia developed pulmonary hypertension, right ventricular diastolic and systolic functions were enhanced in rats, such as the mean pulmonary artery pressure, systolic pressure of pulmonary artery, the max pressure of right ventricular, the mean right ventricular pressure, and the heart rate was significantly higher than that in control. We found that Hif-1 signaling pathway and p38-MAPK signaling pathway have been activated by hypoxia, and cardiomyocyte apoptosis also aggravated in the right ventricular, which might be one cause of cardiomyocyte hypertrophy and myocardial injury, and targeted intervention might be one potential prevention for cardiomyocyte hypertrophy and myocardial injury induced by hypoxia.

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Drag-reducing polymers attenuates pulmonary vascular remodeling and right ventricular dysfunction in a rat model of chronic hypoxia-induced pulmonary hypertension

Cited by 4 publications

References 31 publications

Oxidative Stress, Kinase Activity and Inflammatory Implications in Right Ventricular Hypertrophy and Heart Failure under Hypobaric Hypoxia

Oxidative Stress, Kinase Activity and Inflammatory Implications in Right Ventricular Hypertrophy and Heart Failure under Hypobaric Hypoxia

Calpain‐1 mediates vascular remodelling and fibrosis via HIF‐1α in hypoxia‐induced pulmonary hypertension

Hypoxia-Induced Cardiomyocyte Apoptosis Exacerbates Cardiomyocyte Hypertrophy and Myocardial Injury through p38 MAPK Pathway in SD Rats

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