Journal ArticleDOI
The effects of cooking oil fumes-derived PM2.5 on blood vessel formation through ROS-mediated NLRP3 inflammasome pathway in human umbilical vein endothelial cells.
Chaowei Shen,Jie Liu,Furong Zhu,Ruoqian Lei,Han Cheng,Chao Zhang,Xinmiao Sui,Liu Ding,Mei Yang,Hongbo Chen,Rui Ding,Jiyu Cao +11 more
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TLDR
It was revealed that the impact caused by COFs-derived PM2.5 on blood vessel formation through a ROS-mediated NLRP3 inflammasome pathway could significantly reduce HUVECs viability, induce the overproduction of ROS, lead to inflammation and inhibit VEGF expression, thus affect angiogenesis of HUVES in vitro.About:
This article is published in Ecotoxicology and Environmental Safety.The article was published on 2019-06-15. It has received 32 citations till now. The article focuses on the topics: Tube formation & Inflammasome.read more
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Journal ArticleDOI
New Approach Methods to Evaluate Health Risks of Air Pollutants: Critical Design Considerations for In Vitro Exposure Testing.
Jose Zavala,Anastasia N. Freedman,John T Szilagyi,Ilona Jaspers,John F. Wambaugh,Mark Higuchi,Julia E. Rager +6 more
TL;DR: This review aims to outline important design parameters to consider when using in vitro methods to evaluate air pollutant toxicity, with the goal of providing increased accuracy, reproducibility, and effectiveness when incorporating in vitro data into human health evaluations.
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The critical role of endothelial function in fine particulate matter-induced atherosclerosis.
Shuang Liang,Jingyi Zhang,Ruihong Ning,Zhou Du,Jiangyan Liu,Joe Werelagi Batibawa,Junchao Duan,Zhiwei Sun +7 more
TL;DR: The main mechanisms of PM 2.5 -triggered vascular endothelial injury mainly involved three aspects, including vascular endothelium permeability, vasomotor function and vascular reparative capacity, and the relationship between PM2.5 and atherosclerosis was reviewed.
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Airborne particulate matter (PM2.5) triggers cornea inflammation and pyroptosis via NLRP3 activation
Liangliang Niu,Liping Li,Chao Xing,Bin Luo,Chunchun Hu,Maomao Song,Jingping Niu,Ye Ruan,Xinghuai Sun,Yuan Lei +9 more
TL;DR: Novel evidence is provids that PM2.5 induces corneal toxicity by triggering cell pyroptosis by activating NLRP3 inflammasome-mediated pyroPTosis axis in PM 2.5-treated HCECs, accompanied by increased ROS formation.
Journal ArticleDOI
Airborne particulate matter (PM 2.5 ) triggers ocular hypertension and glaucoma through pyroptosis.
Liping Li,Chao Xing,Ji Zhou,Liangliang Niu,Bin Luo,Maomao Song,Jingping Niu,Ye Ruan,Xinghuai Sun,Yuan Lei +9 more
TL;DR: In this paper, the authors investigated the impact of PM2.5 on intraocular pressure (IOP) and the associated mechanism, C57BL/6 mouse eyes were topically exposed to a PM 2.5 suspension for 3 months, and human trabecular meshwork (HTM) cells were subjected to various PM 2.5 concentrations in vitro.
Journal ArticleDOI
Environmental exposure to cadmium impairs fetal growth and placental angiogenesis via GCN-2-mediated mitochondrial stress
Yong-Wei Xiong,Xiao-Feng Xu,Hua-Long Zhu,Xue-Lin Cao,Song-Jia Yi,Xue-Ting Shi,Kai-Heng Zhu,Yuan Nan,Ling-Li Zhao,Chen Zhang,Lan Gao,Yuan-Hua Chen,De-Xiang Xu,Hua Wang +13 more
TL;DR: Environmental exposure to Cd impairs fetal growth and placental angiogenesis via GCN-2-mediated mitochondrial stress and its mechanism using in vitro and in vivo models.
References
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Journal ArticleDOI
The structural and functional effects of fine particulate matter from cooking oil fumes on rat umbilical cord blood vessels
TL;DR: The results indicated that exposure to COFs-derived PM2.5 was associated with adverse pregnancy outcomes, changed the structure of umbilical cord blood vessels, decreased the diameter and lumen area, and increased wall thickness, and a significant increase of maximum contraction tension was observed in the early pregnancy high-dose exposure group and pregnant low-dose Exposure group compared to the control group.
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[PM2.5 induces oxidative damage and affects nuclear factor-erythroid 2 related factor 2 pathway in human umbilical vein endothelial cells].
TL;DR: It is demonstrated that PM2.5 can lead to oxidative damage to HUVEC in a concentration-dependent manner, and this mechanism may be related to increases in cellular ROS induced by PM 2.5.