Role of inflammation, immunity, and oxidative stress in hypertension: New insights and potential therapeutic targets
Hypertension is regarded as the most prominent risk factor for cardiovascular diseases, which have become a primary cause of death, and recent research has demonstrated that chronic inflammation is involved in the pathogenesis of hypertension. Both innate and adaptive immunity are now known to promo...
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| Vydáno v: | Frontiers in immunology Ročník 13; s. 1098725 |
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| Hlavní autoři: | , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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Switzerland
Frontiers Media S.A
10.01.2023
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| ISSN: | 1664-3224, 1664-3224 |
| On-line přístup: | Získat plný text |
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| Abstract | Hypertension is regarded as the most prominent risk factor for cardiovascular diseases, which have become a primary cause of death, and recent research has demonstrated that chronic inflammation is involved in the pathogenesis of hypertension. Both innate and adaptive immunity are now known to promote the elevation of blood pressure by triggering vascular inflammation and microvascular remodeling. For example, as an important part of innate immune system, classically activated macrophages (M1), neutrophils, and dendritic cells contribute to hypertension by secreting inflammatory cy3tokines. In particular, interferon-gamma (IFN-γ) and interleukin-17 (IL-17) produced by activated T lymphocytes contribute to hypertension by inducing oxidative stress injury and endothelial dysfunction. However, the regulatory T cells and alternatively activated macrophages (M2) may have a protective role in hypertension. Although inflammation is related to hypertension, the exact mechanisms are complex and unclear. The present review aims to reveal the roles of inflammation, immunity, and oxidative stress in the initiation and evolution of hypertension. We envisage that the review will strengthen public understanding of the pathophysiological mechanisms of hypertension and may provide new insights and potential therapeutic strategies for hypertension. |
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| AbstractList | Hypertension is regarded as the most prominent risk factor for cardiovascular diseases, which have become a primary cause of death, and recent research has demonstrated that chronic inflammation is involved in the pathogenesis of hypertension. Both innate and adaptive immunity are now known to promote the elevation of blood pressure by triggering vascular inflammation and microvascular remodeling. For example, as an important part of innate immune system, classically activated macrophages (M1), neutrophils, and dendritic cells contribute to hypertension by secreting inflammatory cy3tokines. In particular, interferon-gamma (IFN-γ) and interleukin-17 (IL-17) produced by activated T lymphocytes contribute to hypertension by inducing oxidative stress injury and endothelial dysfunction. However, the regulatory T cells and alternatively activated macrophages (M2) may have a protective role in hypertension. Although inflammation is related to hypertension, the exact mechanisms are complex and unclear. The present review aims to reveal the roles of inflammation, immunity, and oxidative stress in the initiation and evolution of hypertension. We envisage that the review will strengthen public understanding of the pathophysiological mechanisms of hypertension and may provide new insights and potential therapeutic strategies for hypertension. Hypertension is regarded as the most prominent risk factor for cardiovascular diseases, which have become a primary cause of death, and recent research has demonstrated that chronic inflammation is involved in the pathogenesis of hypertension. Both innate and adaptive immunity are now known to promote the elevation of blood pressure by triggering vascular inflammation and microvascular remodeling. For example, as an important part of innate immune system, classically activated macrophages (M1), neutrophils, and dendritic cells contribute to hypertension by secreting inflammatory cy3tokines. In particular, interferon-gamma (IFN-γ) and interleukin-17 (IL-17) produced by activated T lymphocytes contribute to hypertension by inducing oxidative stress injury and endothelial dysfunction. However, the regulatory T cells and alternatively activated macrophages (M2) may have a protective role in hypertension. Although inflammation is related to hypertension, the exact mechanisms are complex and unclear. The present review aims to reveal the roles of inflammation, immunity, and oxidative stress in the initiation and evolution of hypertension. We envisage that the review will strengthen public understanding of the pathophysiological mechanisms of hypertension and may provide new insights and potential therapeutic strategies for hypertension.Hypertension is regarded as the most prominent risk factor for cardiovascular diseases, which have become a primary cause of death, and recent research has demonstrated that chronic inflammation is involved in the pathogenesis of hypertension. Both innate and adaptive immunity are now known to promote the elevation of blood pressure by triggering vascular inflammation and microvascular remodeling. For example, as an important part of innate immune system, classically activated macrophages (M1), neutrophils, and dendritic cells contribute to hypertension by secreting inflammatory cy3tokines. In particular, interferon-gamma (IFN-γ) and interleukin-17 (IL-17) produced by activated T lymphocytes contribute to hypertension by inducing oxidative stress injury and endothelial dysfunction. However, the regulatory T cells and alternatively activated macrophages (M2) may have a protective role in hypertension. Although inflammation is related to hypertension, the exact mechanisms are complex and unclear. The present review aims to reveal the roles of inflammation, immunity, and oxidative stress in the initiation and evolution of hypertension. We envisage that the review will strengthen public understanding of the pathophysiological mechanisms of hypertension and may provide new insights and potential therapeutic strategies for hypertension. |
| Author | Zhou, Xingyu Zhang, Zenglei Zhao, Lin Meng, Xu Zhou, Xianliang |
| AuthorAffiliation | Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College , Beijing , China |
| AuthorAffiliation_xml | – name: Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College , Beijing , China |
| Author_xml | – sequence: 1 givenname: Zenglei surname: Zhang fullname: Zhang, Zenglei – sequence: 2 givenname: Lin surname: Zhao fullname: Zhao, Lin – sequence: 3 givenname: Xingyu surname: Zhou fullname: Zhou, Xingyu – sequence: 4 givenname: Xu surname: Meng fullname: Meng, Xu – sequence: 5 givenname: Xianliang surname: Zhou fullname: Zhou, Xianliang |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/36703963$$D View this record in MEDLINE/PubMed |
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| IngestDate | Fri Oct 03 12:45:57 EDT 2025 Thu Aug 21 18:38:37 EDT 2025 Fri Sep 05 12:24:10 EDT 2025 Mon Jul 21 06:04:55 EDT 2025 Sat Nov 29 03:32:06 EST 2025 Tue Nov 18 22:44:25 EST 2025 |
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| Keywords | cytokines cardiovascular diseases immunity inflammation hypertension oxidative stress |
| Language | English |
| License | Copyright © 2023 Zhang, Zhao, Zhou, Meng and Zhou. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 Reviewed by: Alberto N. Peón, Sociedad Española de Beneficencia, Mexico; Aisah Aniisah Aubdool, Queen Mary University of London, United Kingdom Edited by: Jianmin Chen, Queen Mary University of London, United Kingdom These authors have contributed equally to this work This article was submitted to Inflammation, a section of the journal Frontiers in Immunology |
| OpenAccessLink | https://doaj.org/article/4e32b62499ed4d87b57485c7eef741b5 |
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| PublicationCentury | 2000 |
| PublicationDate | 2023-01-10 |
| PublicationDateYYYYMMDD | 2023-01-10 |
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| PublicationTitle | Frontiers in immunology |
| PublicationTitleAlternate | Front Immunol |
| PublicationYear | 2023 |
| Publisher | Frontiers Media S.A |
| Publisher_xml | – name: Frontiers Media S.A |
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| Title | Role of inflammation, immunity, and oxidative stress in hypertension: New insights and potential therapeutic targets |
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