Silica nanoparticles induce cardiac injury and dysfunction via ROS/Ca2+/CaMKII signaling

化学 活性氧 氧化应激 细胞凋亡 内科学 背景(考古学) 纤维化 细胞内 内分泌学 线粒体 细胞生物学 医学 生物 生物化学 古生物学
作者
Yi Qi,Hailin Xu,Xueyan Li,Xinying Zhao,Yan Li,Xianqing Zhou,Siyu Chen,Ning Shen,Rui Chen,Yanbo Li,Zhiwei Sun,Caixia Guo,Zhiwei Sun,Caixia Guo
出处
期刊:Science of The Total Environment [Elsevier BV]
卷期号:837: 155733-155733 被引量:39
标识
DOI:10.1016/j.scitotenv.2022.155733
摘要

Interest is growing to better comprehend the interaction of silica nanoparticles (SiNPs) with the cardiovascular system. In particular, the extremely small size, relatively large surface area and associated unique properties may greatly enhance its toxic potentials compared to larger-sized counterparts. Nevertheless, the underlying mechanisms still need to be evaluated. In this context, the cardiotoxicity of nano-scale (Si-60; particle diameter about 60 nm) and submicro-scale silica particles (Si-300; 300 nm) were examined in ApoE-/- mice via intratracheal instillation, 6.0 mg/kg·bw, once per week for 12 times. The echocardiography showed that the sub-chronic exposure of Si-60 declined cardiac output (CO) and stroke volume (SV), shorten LVIDd and LVIDs, and thickened LVAWs of ApoE-/- mice in compared to the control and Si-300 groups. Histological investigations manifested Si-60 enhanced inflammatory infiltration, myocardial fiber arrangement disorder, hypertrophy and fibrosis in the cardiac tissue, as well as mitochondrial ultrastructural injury. Accordingly, the serum cTnT, cTnI and ANP were significantly elevated by Si-60, as well as cardiac ANP content. In particular, Si-60 greatly increased cardiac ROS, Ca2+ levels and CaMKII activation in comparison with Si-300. Further, in vitro investigations revealed silica particles induced a dose- and size-dependent activation of oxidative stress, mitochondrial membrane permeabilization, intracellular Ca2+ overload, CaMKII signaling activation and ensuing myocardial apoptosis in human cardiomyocytes (AC16). Mechanistic analyses revealed SiNPs induced myocardial apoptosis via ROS/Ca2+/CaMKII signaling, which may contribute to the abnormalities in cardiac structure and function in vivo. In summary, our research revealed SiNPs caused myocardial impairments, dysfunction and even structural remodeling via ROS/Ca2+/CaMKII signaling. Of note, a size-dependent myocardial toxicity was noticed, that is, Si-60 greater than Si-300.
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
刚刚
刚刚
无情向秋发布了新的文献求助10
1秒前
FashionBoy应助空中马铃薯采纳,获得10
2秒前
2秒前
愉快草莓完成签到,获得积分10
3秒前
小雨完成签到,获得积分10
3秒前
5秒前
7秒前
7秒前
JamesPei应助Seagull采纳,获得10
8秒前
顺利的绿柏完成签到,获得积分10
8秒前
9秒前
10秒前
小顾发布了新的文献求助10
11秒前
11秒前
11秒前
11秒前
幸运小狗关注了科研通微信公众号
12秒前
sk夏冰完成签到 ,获得积分10
12秒前
ZZZ完成签到,获得积分10
12秒前
稀饭发布了新的文献求助10
13秒前
13秒前
14秒前
赵爽发布了新的文献求助10
14秒前
15秒前
Nice发布了新的文献求助10
15秒前
15秒前
MattZ完成签到,获得积分10
16秒前
16秒前
小巧水绿发布了新的文献求助10
16秒前
满意的慕凝完成签到,获得积分10
17秒前
17秒前
yu发布了新的文献求助10
18秒前
19秒前
19秒前
19秒前
积极便当发布了新的文献求助10
19秒前
星辰大海应助苏丹烟采纳,获得10
20秒前
张林夕发布了新的文献求助10
21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
Nondestructive Testing Handbook: Vol. 4, Thermal and Infrared Testing (IR), 4th ed 800
作者名:Kristopher P. Plain,悉尼大学的,目前只能查到其四篇论文,想找到其博士论文 590
Évora na Idade Média 555
Soil mites of the family Rhagidiidae (Actinedida: Eupodoidea). Morphology, Systematics, Ecology 520
Matrix Methods in Data Mining and Pattern Recognition Second Edition 510
Stratospheric Ozone: A Textbook 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 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 7360105
求助须知:如何正确求助?哪些是违规求助? 8969881
关于积分的说明 19064991
捐赠科研通 7006804
什么是DOI,文献DOI怎么找? 3223067
关于科研通互助平台的介绍 2386875
邀请新用户注册赠送积分活动 2203885