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Review
. 2023 Apr 28;21(1):140.
doi: 10.1186/s12951-023-01899-y.

Insights into the toxicological effects of nanomaterials on atherosclerosis: mechanisms involved and influence factors

Siyu Chen  1 , Yuan Su  2 , Manjin Zhang  3 , Yulin Zhang  3 , Peiming Xiu  4 , Wei Luo  1 , Qiuxia Zhang  1 , Xinlu Zhang  1 , Hongbin Liang  1 , Alex Pui-Wai Lee  5 , Longquan Shao  6 , Jiancheng Xiu  7
Affiliations
Review

Insights into the toxicological effects of nanomaterials on atherosclerosis: mechanisms involved and influence factors

Siyu Chen et al. J Nanobiotechnology. .

Abstract

Atherosclerosis is one of the most common types of cardiovascular disease and is driven by lipid accumulation and chronic inflammation in the arteries, which leads to stenosis and thrombosis. Researchers have been working to design multifunctional nanomedicines with the ability to target, diagnose, and treat atherosclerosis, but recent studies have also identified that nanomaterials can cause atherosclerosis. Therefore, this review aims to outline the molecular mechanisms and physicochemical properties of nanomaterials that promote atherosclerosis. By analyzing the toxicological effects of nanomaterials on cells involved in the pathogenesis of atherosclerosis such as vascular endothelial cells, vascular smooth muscle cells and immune cells, we aim to provide new perspectives for the prevention and treatment of atherosclerosis, and raise awareness of nanotoxicology to advance the clinical translation and sustainable development of nanomaterials.

Keywords: Atherosclerosis; Endothelial cell; Immune cell; Nanomaterials; Nanotoxicology; Smooth muscle cell.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
CD68 (a and b), Perl’s (c and d), and CD68/Perl’s (e) double staining of the endarterectomy specimen of a patient who received USPIOs. The red coloring (a and b) and brown coloring (e) are indicative of macrophages, and the blue coloring (c, d, and e) is indicative of the accumulation of USPIOs. The double lumen is indicated with L, the surgical cut with C, and tears with T [7]. Copyright © 2003, Wolters Kluwer Health
Fig. 2
Fig. 2
Schematic of the main mechanisms of NM-induced endothelial leakage. NMs cause endothelial leakage by disrupting VE-cadherin, claudins and occludin and inducing actin rearrangements, leading to subsequent exudation of LDL and leukocytes
Fig. 3
Fig. 3
Schematic of the main mechanisms of NM-induced phenotype switching. NMs promote VSMCs from the contractile type to foam cells, macrophage-like VSMCs, and osteoblast-like VSMCs
Fig. 4
Fig. 4
ER stress-mediated the upregulated CD36 expression attributed to the lipid accumulation induced by SiNPs in RAW264.7 cells. A The relative mRNA expression of factors involved in cholesterol influx/efflux. b CD36 protein expression in RAW264.7 cells. Consistent with the mRNA level, the upregulated CD36 expression induced by SiNPs was greatly alleviated by 4-PBA pretreatment (an ER stress inhibitor). c CD36 expression in the plaques of SiNP-exposed aortic roots was upregulated [171]. No Copyright
Fig. 5
Fig. 5
Effects of PLGA NPs and their protein coronas on the transformation of macrophages into foam cells. A, b Effects of PLGA NPs and PLGA + PC on the phagocytosis of ox-LDL by Raw 264.7 macrophages. C The CE/TC (%) of macrophages to foam cells after treatment with NPs [19]. No Copyright
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