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Special Issue Editors

Dr. Guoqing Zhu

Department of Physiology, Nanjing Medical University, Nanjing 210029, China
Interests: hypertension; cardiovascular; sympathetic activity; exosome; vascular remodeling

Dr. Ye-Bo Zhou

E-Mail Website
Guest Editor

Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center of Translational Medicine for Cardiovascular Disease, and Department of Physiology, Nanjing Medical University, Nanjing 211166, China
Interests: hypertension; vascular remodeling; vasoactive peptide; obesity; calcification; inflammation

Dr. Ying Han

E-Mail Website
Guest Editor

Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center of Translational Medicine for Cardiovascular Disease, and Department of Physiology, Nanjing Medical University, Nanjing 211166, China
Interests: hypertension; vascular remodeling; vascular smooth muscle cells, proliferation; migration; signaling

Special Issue Information

Dear Colleagues,

Vascular remodeling contributes to the development and complications of hypertension. Regression of vascular remodeling may be an important therapeutic strategy for hypertension, especially for reducing the incidence of cardiovascular events such as stroke, myocardial infarction, and end-organ damage.

In hypertension, vascular remodeling involves changes in structure and functions, including vascular smooth muscle cells (VSMCs) and other cellular components, such as adventitial fibroblasts, endothelial cells, and elastin and collagen content in the vascular wall of large and small arteries. Lots of bioactive molecules and their downstream signals constitute complex networks, impacting cell proliferation, migration, apoptosis and autophagy, matrix formation and fibrosis, and oxidative stress and inflammation and eventually contributing to vascular remodeling. The interaction of cells in the vessels makes the network more complex.

This Special Issue is focused on recent advances in the molecular mechanism of vascular remodeling in hypertension, from pathophysiology to therapeutic targets. We invite authors to submit original research articles or review articles relating to the theme.

Dr. Guoqing Zhu
Dr. Ye-Bo Zhou
Dr. Ying Han
Guest Editors

Manuscript Submission Information

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Keywords

hypertension
vascular remodeling
oxidative stress
inflammation
extracellular vesicles
vasoactive peptides

Published Papers (2 papers)

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Research

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18 pages, 3878 KiB

Open AccessArticle

miR-31-5p Promotes Oxidative Stress and Vascular Smooth Muscle Cell Migration in Spontaneously Hypertensive Rats via Inhibiting FNDC5 Expression

by Bing Zhou, Lu-Lu Wu, Fen Zheng, Nan Wu, Ai-Dong Chen, Hong Zhou, Jing-Yu Chen, Qi Chen, Yue-Hua Li, Yu-Ming Kang and Guo-Qing Zhu

Biomedicines 2021, 9(8), 1009; https://doi.org/10.3390/biomedicines9081009 - 13 Aug 2021

Cited by 16 | Viewed by 2302

Abstract

Oxidative stress and the migration of vascular smooth muscle cells (VSMCs) are important for vascular remodeling in a variety of vascular diseases. miR-31-5p promotes cell migration in colorectal cancer cells but inhibits cell migration in renal cell carcinoma. However, whether miR-31-5p is involved in oxidative stress and VSMC migration remains unknown. This study shows the crucial roles of miR-31-5p in oxidative stress and VSMC migration, as well as underlying mechanisms. Experiments were carried out in primary VSMCs from aortic media of Wistar–Kyoto rats (WKY) and spontaneously hypertensive rats (SHR), as well as the A7r5 cell line. Oxidative stress was assessed by NADPH oxidase (NOX) expression, NOX activity, and reactive oxygen species (ROS) production. Cell migration was evaluated with a Boyden chamber assay and a wound healing assay. The miR-31-5p mimic and inhibitor promoted and attenuated oxidative stress and cell migration in the VSMCs of SHR, respectively. A dual-luciferase reporter assay indicated that miR-31-5p targeted the 3’UTR domain of FNDC5. The miR-31-5p level was raised and FNDC5 expression was reduced in the VSMCs of SHR compared with those of WKY. The miR-31-5p mimic reduced FNDC5 expression in the A7r5 cells and the VSMCs of both WKY and SHR, while the miR-31-5p inhibitor only increased FNDC5 expression in the VSMCs of SHR. Exogenous FNDC5 attenuated not only the oxidative stress and VSMC migration in SHR but also the roles of the miR-31-5p mimic in inducing oxidative stress and VSMC migration. These results indicate that miR-31-5p promotes oxidative stress and VSMC migration in SHR via inhibiting FNDC5 expression. The increased miR-31-5p and reduced FNDC5 in the VSMCs of SHR contribute to enhanced oxidative stress and cell migration. Full article

(This article belongs to the Special Issue Vascular Remodeling in Hypertension: From Pathophysiology to Therapeutic Targets)

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Review

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23 pages, 1633 KiB

Open AccessReview

Mitochondrial Metabolism, Redox, and Calcium Homeostasis in Pulmonary Arterial Hypertension

by Shuxin Liang, Manivannan Yegambaram, Ting Wang, Jian Wang, Stephen M. Black and Haiyang Tang

Biomedicines 2022, 10(2), 341; https://doi.org/10.3390/biomedicines10020341 - 1 Feb 2022

Cited by 17 | Viewed by 5137

Abstract

Pulmonary arterial hypertension (PAH) is a progressive disease characterized by elevated pulmonary arterial pressure due to increased pulmonary vascular resistance, secondary to sustained pulmonary vasoconstriction and excessive obliterative pulmonary vascular remodeling. Work over the last decade has led to the identification of a critical role for metabolic reprogramming in the PAH pathogenesis. It is becoming clear that in addition to its role in ATP generation, the mitochondrion is an important organelle that regulates complex and integrative metabolic- and signal transduction pathways. This review focuses on mitochondrial metabolism alterations that occur in deranged pulmonary vessels and the right ventricle, including abnormalities in glycolysis and glucose oxidation, fatty acid oxidation, glutaminolysis, redox homeostasis, as well as iron and calcium metabolism. Further understanding of these mitochondrial metabolic mechanisms could provide viable therapeutic approaches for PAH patients. Full article

(This article belongs to the Special Issue Vascular Remodeling in Hypertension: From Pathophysiology to Therapeutic Targets)

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