Modulating Plaque Inflammation via Targeted mRNA Nanoparticles for the Treatment of Atherosclerosis

炎症 巨噬细胞 医学 纤维帽 阿托伐他汀 免疫学 病理 药理学 生物 体外 生物化学
作者
Mingzhu Gao,Maoping Tang,William Ho,Yilong Teng,Qijing Chen,Lei Bu,Xiaoyang Xu,Xue‐Qing Zhang
出处
期刊:ACS Nano [American Chemical Society]
卷期号:17 (18): 17721-17739 被引量:101
标识
DOI:10.1021/acsnano.3c00958
摘要

Atherosclerosis is a common pathology present in many cardiovascular diseases. Although the current therapies (including statins and inhibitors of the serine protease PCSK9) can effectively reduce low-density lipoprotein (LDL) cholesterol levels to guideline-recommended levels, major adverse cardiovascular events still occur frequently. Indeed, the subendothelial retention of lipoproteins in the artery wall triggers multiple events of inflammation in macrophages and is a major contributor to the pathological progression of atherosclerosis. It has been gradually recognized that modulating inflammation is, therefore, an attractive avenue to forestall and treat atherosclerosis and its complications. Unfortunately, challenges with specificity and efficacy in managing plaque inflammation have hindered progress in atherosclerosis treatment. Herein, we report an NP-mediated mRNA therapeutic approach to target atherosclerotic lesional macrophages, modulating inflammation in advanced atherosclerotic lesions for the treatment of atherosclerosis. We demonstrated that the targeted NPs containing IL-10 mRNA colocalized with M2-like macrophages and induced IL-10 production in atherosclerotic plaques following intravenous administration to Western diet (WD)-fed Ldlr –/– mice. Additionally, the lesions showed a significantly alleviated inflammatory response, as evidenced by reduced oxidative stress and macrophage apoptosis, resulting in decreased lipid deposition, diminished necrotic areas, and increased fiber cap thickness. These results demonstrate the successful delivery of mRNA therapeutics to macrophage-enriched plaques in a preclinical model of advanced atherosclerosis, showing that this targeted NP inflammation management approach has great potential for translation into a wide range of clinical applications.
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
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
跳跃紫萱发布了新的文献求助10
1秒前
1秒前
1秒前
1秒前
maolihui的应助被小图采纳,获得50
2秒前
无极微光的应助被人间采纳,获得20
3秒前
whw发布了新的文献求助10
3秒前
LEI完成签到,获得积分10
4秒前
百里烬言发布了新的文献求助10
7秒前
白色茉莉花完成签到,获得积分10
7秒前
8秒前
9秒前
JamesPei的应助被111采纳,获得10
9秒前
星际战完成签到,获得积分10
10秒前
jctyp发布了新的文献求助10
10秒前
Ame完成签到,获得积分10
10秒前
SciGPT的应助被LEI采纳,获得10
10秒前
10秒前
bemyselfelsa完成签到,获得积分10
11秒前
wanci的应助被yy采纳,获得10
12秒前
15秒前
xft发布了新的文献求助10
16秒前
18秒前
18秒前
辛勤鼠标完成签到,获得积分20
21秒前
光亮的初丹完成签到,获得积分10
22秒前
23秒前
23秒前
嘻嘻完成签到,获得积分10
25秒前
Akim的应助被呆萌安萱采纳,获得10
26秒前
芝士就是力量完成签到,获得积分10
26秒前
科研通AI6.2的应助被fpc采纳,获得10
27秒前
28秒前
29秒前
Dandelion完成签到,获得积分10
29秒前
苏飞完成签到,获得积分10
29秒前
29秒前
北海章完成签到,获得积分10
30秒前
观察者小黑完成签到,获得积分10
32秒前
美丽的小羊完成签到,获得积分10
32秒前
高分求助中
(应助此贴封号)通过应助OA文献获取积分 10000
Rosenblum, Global Change Biology 800
Computational Chemical Reaction Engineering: Modeling, Simulation, and Design with MATLAB 600
Organizational Behavior 510
Management and the Arts 510
Production Logging: Theoretical and Interpretive Elements 400
CLSI C56QG Examples of Hemolyzed, Icteric, and Lipemic/Turbid Samples Quick Guide 400
热门求助领域 (近24小时)
化学 材料科学 医学 生物 计算机科学 工程类 纳米技术 内科学 物理 有机化学 化学工程 生物化学 复合材料 光电子学 细胞生物学 心理学 量子力学 催化作用 物理化学 电极
热门帖子
关注 科研通微信公众号,转发送积分 7814321
求助须知:如何正确求助?哪些是违规求助? 9344564
关于积分的说明 20524135
捐赠科研通 7407231
什么是DOI,文献DOI怎么找? 3330799
关于科研通互助平台的介绍 2477276
邀请新用户注册赠送积分活动 2350374