Research Progress of Inflammatory Factors in Chronic Obstructive Pulmonary Disease with Pulmonary Hypertension at High Altitude.

肺动脉高压 医学 慢性阻塞性肺病 缺氧性肺血管收缩 缺氧(环境) 炎症 发病机制 促炎细胞因子 内皮功能障碍 免疫学 心脏病学 内科学 化学 有机化学 氧气
作者
Hui Huang,Yang Li-mei
出处
期刊:PubMed 卷期号:29 (8): 689-693 被引量:1
链接
标识
摘要

Chronic obstructive pulmonary disease (COPD) is currently one of the highest morbidity and mortality worldwide, a serious public health problem. Pulmonary hypertension is a common complication of COPD. At present, the pathogenesis of pulmonary hypertension is not clear. A concise overview of the known factors contributing to pulmonary hypertension in COPD includes hypoxia and inflammation. Hypoxia, resulting from lung damage and inadequate oxygen supply, can lead to pulmonary vasoconstriction and increased vascular resistance, thus contributing to the development of pulmonary hypertension in COPD patients. Inflammation also plays a significant role in the progression of pulmonary hypertension. COPD patients exhibit inflammatory responses in their lung tissues, with the release of various inflammatory mediators. These mediators can stimulate abnormal proliferation of endothelial cells and smooth muscle cells within the pulmonary arteries, leading to vascular wall thickening and restricted blood flow. This paper focuses on the pathogenesis of four inflammatory factors, namely interleukin (IL-1β), IL-6, IL-8, and tumor necrosis factor (TNF)-α, in pulmonary hypertension. IL-1β, IL-6, IL-8, and TNF-α are known as pro-inflammatory cytokines that play crucial roles in the inflammatory response. In the context of pulmonary hypertension, these inflammatory factors have been implicated in the remodeling of the pulmonary vasculature, leading to increased vascular resistance and impaired blood flow. The research presented in this paper will delve into the current scientific knowledge surrounding IL-1β, IL-6, IL-8, and TNF-α, and their roles in pulmonary vascular remodeling, endothelial dysfunction, smooth muscle cell proliferation, and inflammation. The goal is to provide a comprehensive overview of their involvement in pulmonary hypertension and how these factors may be influenced by the hypoxic environment prevalent in high-altitude regions. By focusing on the relevance of these inflammatory factors in high-altitude areas, we hope to contribute valuable insights that can inform clinical management strategies, prevention approaches, and potential therapeutic interventions for individuals residing in such regions who are at an increased risk of developing pulmonary hypertension.

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
无花果应助啦啦啦采纳,获得10
刚刚
耍酷如柏完成签到,获得积分10
1秒前
东皇太憨完成签到,获得积分0
1秒前
零零柒完成签到 ,获得积分10
2秒前
Wenqi发布了新的文献求助10
2秒前
Jasper应助结实怀莲采纳,获得10
2秒前
柳絮发布了新的文献求助10
3秒前
Gel完成签到,获得积分10
3秒前
顶刊我来了完成签到,获得积分10
3秒前
文艺莹芝发布了新的文献求助10
3秒前
Jasper应助xu采纳,获得10
5秒前
打打应助13456采纳,获得10
5秒前
mashuai完成签到,获得积分10
5秒前
5秒前
良生沿见完成签到,获得积分10
6秒前
6秒前
Mryuan完成签到,获得积分10
7秒前
8秒前
breeze发布了新的文献求助10
8秒前
小猫钓鱼灯完成签到 ,获得积分10
8秒前
8秒前
科研通AI6.3应助W~舞采纳,获得10
9秒前
脑洞疼应助一颗烂番茄采纳,获得10
10秒前
啦啦啦完成签到,获得积分10
10秒前
10秒前
心语完成签到,获得积分10
10秒前
可爱的函函应助蓝天采纳,获得10
10秒前
李爱国应助陈思采纳,获得10
11秒前
Ywffffff发布了新的文献求助10
12秒前
12秒前
xiaonanzi1完成签到,获得积分10
12秒前
bkagyin应助猪皮恶人采纳,获得10
13秒前
啦啦啦发布了新的文献求助10
13秒前
香蕉觅云应助彪壮的夏寒采纳,获得10
13秒前
愉快之槐发布了新的文献求助10
13秒前
13秒前
13秒前
kll完成签到,获得积分10
13秒前
易瑾完成签到 ,获得积分10
14秒前
14秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
AnnualResearch andConsultation Report of Panorama survey and Investment strategy onChinaIndustry 1000
卤化钙钛矿人工突触的研究 1000
Engineering for calcareous sediments : proceedings of the International Conference on Calcareous Sediments, Perth 15-18 March 1988 / edited by R.J. Jewell, D.C. Andrews 1000
Continuing Syntax 1000
Signals, Systems, and Signal Processing 610
2026 Hospital Accreditation Standards 500
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 工程类 有机化学 化学工程 生物化学 计算机科学 物理 内科学 复合材料 催化作用 物理化学 光电子学 电极 细胞生物学 基因 无机化学
热门帖子
关注 科研通微信公众号,转发送积分 6264160
求助须知:如何正确求助?哪些是违规求助? 8085952
关于积分的说明 16898498
捐赠科研通 5334647
什么是DOI,文献DOI怎么找? 2839425
邀请新用户注册赠送积分活动 1816885
关于科研通互助平台的介绍 1670463