Common Pathogeneses Underlying Asthma and Chronic Obstructive Pulmonary Disease -Insights from Genetic Studies

医学 哮喘 慢性阻塞性肺病 发病机制 鼻病毒 炎症 疾病 免疫学 重症监护医学 生物信息学 内科学 病毒 生物
作者
Nobuyuki Hizawa
出处
期刊:International Journal of Chronic Obstructive Pulmonary Disease [Dove Medical Press]
卷期号:Volume 19: 633-642
标识
DOI:10.2147/copd.s441992
摘要

Neither asthma nor chronic obstructive pulmonary disease (COPD) is a single disease consisting of a uniform pathogenesis; rather, they are both syndromes that result from a variety of basic distinct pathogeneses. Many of the basic pathogeneses overlap between the two diseases, and multiple basic pathogeneses are simultaneously involved at varying proportions in individual patients. The specific combination of different basic pathogeneses in each patient determines the phenotype of the patient, and it varies widely from patient to patient. For example, type 2 airway inflammation and neutrophilic airway inflammation may coexist in the same patient, and quite a few patients have clinical characteristics of both asthma and COPD. Even in the same patient, the contribution of each pathogenesis is expected to differ at different life stages (eg, childhood, adolescence, middle age, and older), during different seasons (eg, high seasons for hay fever and rhinovirus infection), and depending on the nature of treatments. This review describes several basic pathogeneses commonly involved in both asthma and COPD, including chronic non-type 2 inflammation, type 2 inflammation, viral infections, and lung development. Understanding of the basic molecular pathogeneses in individual patients, rather than the use of clinical diagnosis, such as asthma, COPD, or even asthma COPD overlap, will enable us to better deal with the diversity seen in disease states, and lead to optimal treatment practices tailored for each patient with less disease burden, such as drug-induced side effects, and improved prognosis. Furthermore, we can expect to focus on these molecular pathways as new drug discovery targets.

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
下雨天的树完成签到,获得积分10
刚刚
冷吃兔要热了吃完成签到,获得积分10
刚刚
生动的雅绿完成签到 ,获得积分10
1秒前
hala安胖胖完成签到,获得积分10
1秒前
吹泡泡完成签到 ,获得积分10
1秒前
小霞完成签到 ,获得积分10
1秒前
boyang发布了新的文献求助30
1秒前
2秒前
2秒前
脑洞疼应助挽风风风风采纳,获得10
2秒前
活泼的大船完成签到,获得积分0
3秒前
行洲完成签到,获得积分10
3秒前
天穹雨应助跳跃的访曼采纳,获得20
3秒前
满意的寒凝完成签到 ,获得积分10
3秒前
虞访云发布了新的文献求助10
4秒前
小牧鱼完成签到,获得积分10
4秒前
WWWW完成签到,获得积分10
4秒前
4秒前
难过冰萍完成签到,获得积分10
4秒前
风铃夜雨完成签到 ,获得积分10
5秒前
7秒前
鲤鱼野狼完成签到,获得积分10
7秒前
7秒前
winni完成签到,获得积分10
7秒前
呵呵呵呵柳完成签到,获得积分10
8秒前
海海完成签到,获得积分10
8秒前
8秒前
飞想思完成签到,获得积分10
9秒前
洁净灭男完成签到,获得积分10
9秒前
深情安青应助福多多采纳,获得10
11秒前
祖安诳人完成签到,获得积分10
11秒前
fairy发布了新的文献求助10
12秒前
海风发布了新的文献求助10
12秒前
YY完成签到,获得积分10
13秒前
风趣的灵松完成签到,获得积分10
13秒前
13秒前
桐桐应助花凉采纳,获得10
13秒前
明理的机器猫完成签到,获得积分10
14秒前
xixi完成签到 ,获得积分10
14秒前
15秒前
高分求助中
Principles of Economics, 11th Edition 10000
University Physics with Modern Physics, 16th edition 10000
(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
Arthritis and Related Conditions, An Issue of Orthopedic Clinics 1000
Development of a Bridge Weigh-In-Motion System: A technology to convert the bridge response to the passage of traffic into data on vehicle configurations, speeds, times of travel and weights 1000
ズームレンズの光学設計に関する研究 800
Fundamentals of Pharmaceutical and Biologics Regulations: A Global Perspective, Second Edition 700
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 内科学 物理 复合材料 催化作用 细胞生物学 无机化学 光电子学 物理化学 电极 基因
热门帖子
关注 科研通微信公众号,转发送积分 7290957
求助须知:如何正确求助?哪些是违规求助? 8909968
关于积分的说明 18858046
捐赠科研通 6958147
什么是DOI,文献DOI怎么找? 3209203
关于科研通互助平台的介绍 2378989
邀请新用户注册赠送积分活动 2184966