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
刚刚
打打应助老武采纳,获得10
1秒前
南汐完成签到,获得积分10
2秒前
dy发布了新的文献求助10
2秒前
黎智宸发布了新的文献求助10
2秒前
单薄凌晴完成签到,获得积分10
3秒前
3秒前
复杂语山完成签到,获得积分10
4秒前
LEO完成签到 ,获得积分10
4秒前
xinyi发布了新的文献求助30
5秒前
张博发布了新的文献求助10
5秒前
vetgmy完成签到,获得积分10
5秒前
纸鸟发布了新的文献求助10
5秒前
niNe3YUE应助phy采纳,获得10
6秒前
加油吧科研完成签到,获得积分10
6秒前
聪明新筠完成签到,获得积分10
6秒前
7秒前
8秒前
liuwenjie应助LLLL采纳,获得10
8秒前
菜鸡上线发布了新的文献求助10
8秒前
Ava应助LLLL采纳,获得10
8秒前
HAL9000完成签到,获得积分10
9秒前
蓝莓橘子酱应助单薄凌晴采纳,获得10
9秒前
9秒前
LEGION应助晓槐采纳,获得10
9秒前
神勇的惜文完成签到,获得积分20
10秒前
华仔应助风清扬采纳,获得10
11秒前
11秒前
zhutae完成签到 ,获得积分10
11秒前
一行发布了新的文献求助20
11秒前
egg发布了新的文献求助10
13秒前
无花果应助林夕夕采纳,获得10
13秒前
13秒前
生物钟发布了新的文献求助10
13秒前
小八统治世界完成签到,获得积分10
14秒前
popdragon发布了新的文献求助10
14秒前
阔达的莫言完成签到,获得积分10
16秒前
老北京发布了新的文献求助10
16秒前
16秒前
今夕发布了新的文献求助20
16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
Modern Epidemiology, Fourth Edition 5000
Handbook of pharmaceutical excipients, Ninth edition 5000
Digital Twins of Advanced Materials Processing 2000
Weaponeering, Fourth Edition – Two Volume SET 2000
Polymorphism and polytypism in crystals 1000
Signals, Systems, and Signal Processing 610
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 纳米技术 有机化学 生物化学 化学工程 物理 计算机科学 复合材料 内科学 催化作用 物理化学 光电子学 电极 冶金 基因 遗传学
热门帖子
关注 科研通微信公众号,转发送积分 6022608
求助须知:如何正确求助?哪些是违规求助? 7643263
关于积分的说明 16169884
捐赠科研通 5170921
什么是DOI,文献DOI怎么找? 2766913
邀请新用户注册赠送积分活动 1750251
关于科研通互助平台的介绍 1636941