MiR-223-3p in Cardiovascular Diseases: A Biomarker and Potential Therapeutic Target.

小RNA 生物标志物 内科学 疾病 生物信息学
作者
Meng-Wan Zhang,Yun-Jie Shen,Jing Shi,Jian-Guang Yu
出处
期刊:Frontiers in Cardiovascular Medicine [Frontiers Media SA]
卷期号:7: 610561-610561 被引量:5
标识
DOI:10.3389/fcvm.2020.610561
摘要

Cardiovascular diseases, involving vasculopathy, cardiac dysfunction, or circulatory disturbance, have become the major cause of death globally and brought heavy social burdens. The complexity and diversity of the pathogenic factors add difficulties to diagnosis and treatment, as well as lead to poor prognosis of these diseases. MicroRNAs are short non-coding RNAs to modulate gene expression through directly binding to the 3'-untranslated regions of mRNAs of target genes and thereby to downregulate the protein levels post-transcriptionally. The multiple regulatory effects of microRNAs have been investigated extensively in cardiovascular diseases. MiR-223-3p, expressed in multiple cells such as macrophages, platelets, hepatocytes, and cardiomyocytes to modulate their cellular activities through targeting a variety of genes, is involved in the pathological progression of many cardiovascular diseases. It participates in regulation of several crucial signaling pathways such as phosphatidylinositol 3-kinase/protein kinase B, insulin-like growth factor 1, nuclear factor kappa B, mitogen-activated protein kinase, NOD-like receptor family pyrin domain containing 3 inflammasome, and ribosomal protein S6 kinase B1/hypoxia inducible factor 1 α pathways to affect cell proliferation, migration, apoptosis, hypertrophy, and polarization, as well as electrophysiology, resulting in dysfunction of cardiovascular system. Here, in this review, we will discuss the role of miR-223-3p in cardiovascular diseases, involving its verified targets, influenced signaling pathways, and regulation of cell function. In addition, the potential of miR-223-3p as therapeutic target and biomarker for diagnosis and prediction of cardiovascular diseases will be further discussed, providing clues for clinicians.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
大幅提高文件上传限制,最高150M (2024-4-1)

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
HEIKU应助mmlikeu采纳,获得10
刚刚
haipronl完成签到,获得积分10
1秒前
TingWan发布了新的文献求助10
1秒前
wanci应助余进步采纳,获得10
2秒前
浊酒完成签到,获得积分20
2秒前
BigBadWolf发布了新的文献求助10
2秒前
3秒前
3秒前
时泰发布了新的文献求助10
3秒前
瞿访云发布了新的文献求助10
3秒前
搜集达人应助白凉鞋采纳,获得10
4秒前
Akim应助喷泡的兔子采纳,获得30
4秒前
小夏完成签到,获得积分10
5秒前
5秒前
Shirley给奈奈iii的求助进行了留言
6秒前
wanci应助专一的万怨采纳,获得10
6秒前
王提发布了新的文献求助10
6秒前
武迪完成签到,获得积分10
6秒前
licheng发布了新的文献求助30
8秒前
室内设计发布了新的文献求助10
8秒前
12rcli发布了新的文献求助10
9秒前
9秒前
游标卡尺完成签到,获得积分20
9秒前
耍酷蛋挞完成签到,获得积分10
10秒前
22完成签到,获得积分10
11秒前
勤奋的PRUNUS完成签到,获得积分10
11秒前
11秒前
zy大章鱼完成签到,获得积分10
12秒前
12秒前
英姑应助kyttytk采纳,获得10
12秒前
包妹完成签到,获得积分10
13秒前
彭珊发布了新的文献求助30
14秒前
田様应助求学采纳,获得10
15秒前
Akim应助医平青云采纳,获得10
15秒前
15秒前
fan发布了新的文献求助10
16秒前
Ava应助huizi采纳,获得10
16秒前
自然浩阑发布了新的文献求助100
16秒前
虚心白曼完成签到,获得积分10
16秒前
达达利亚发布了新的文献求助10
17秒前
高分求助中
Sustainability in Tides Chemistry 2800
The Young builders of New china : the visit of the delegation of the WFDY to the Chinese People's Republic 1000
Rechtsphilosophie 1000
Bayesian Models of Cognition:Reverse Engineering the Mind 888
Le dégorgement réflexe des Acridiens 800
Defense against predation 800
Very-high-order BVD Schemes Using β-variable THINC Method 568
热门求助领域 (近24小时)
化学 医学 生物 材料科学 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 基因 遗传学 催化作用 物理化学 免疫学 量子力学 细胞生物学
热门帖子
关注 科研通微信公众号,转发送积分 3135577
求助须知:如何正确求助?哪些是违规求助? 2786454
关于积分的说明 7777484
捐赠科研通 2442441
什么是DOI,文献DOI怎么找? 1298558
科研通“疑难数据库(出版商)”最低求助积分说明 625193
版权声明 600847