Warning on the inhalation of silica nanoparticles: Experimental evidence for its easy passage through the air-blood barrier, resulting in systemic distribution and pathological injuries.

As a result of accumulating data, silica nanoparticles (SiNPs) are known to be harmful when inhaled. Nevertheless, the systemic research on its biological processes remains incompletely understood. In our work, we investigated the systemic effects in rats in response to the respiratory exposure of SiNPs, and in-depth clarified the particle distribution in vivo.

Silica nanoparticles triggered epithelial ferroptosis via miR-21-5p/GCLM signaling to contribute to fibrogenesis in the lungs.

The toxicity of silica nanoparticles (SiNPs) to lung is known. We previously demonstrated that exposure to SiNPs promoted pulmonary impairments, but the precise pathogenesis remains elucidated. Ferroptosis has now been identified as a unique form of oxidative cell death, but whether it participated in SiNPs-induced lung injury remains unclear.

Ferroptosis contributing to cardiomyocyte injury induced by silica nanoparticles via miR-125b-2-3p/HO-1 signaling.

Background: Amorphous silica nanoparticles (SiNPs) have been gradually proven to threaten cardiac health, but pathogenesis has not been fully elucidated. Ferroptosis is a newly defined form of programmed cell death that is implicated in myocardial diseases. Nevertheless, its role in the adverse cardiac effects of SiNPs has not been described.

Amorphous silica nanoparticles caused lung injury through the induction of epithelial apoptosis via ROS/Ca/DRP1-mediated mitochondrial fission signaling.

The adverse effects of amorphous silica nanoparticles (SiNPs) exposure on the respiratory system were increasingly recognized, however, its potential pathogenesis still remains not fully elucidated. So, this study aimed to explore its effects on pulmonary injury, and to investigate related mechanisms. Histological investigations illustrated SiNPs triggered the lung injury, mainly manifested as alveolar structure destruction, collagen deposition, and mitochondrial ultrastructural injury.

Long-term respiratory exposure to amorphous silica nanoparticles promoted systemic inflammation and progression of fibrosis in a susceptible mouse model.

Exposure to amorphous silica nanoparticles (SiNPs) has increased dramatically, and concerns are growing about their potential health effects. However, their long-term systemic toxicity profile and underlying mechanisms following respiratory exposure still remains unexplored. It is well documented that the inhalation of ultrafine particles is firmly associated with adverse effects in humans.

Myocardial toxicity induced by silica nanoparticles in a transcriptome profile.

The deleterious effects of silica nanoparticles (SiNPs) on human health and the ecological system have gradually gained attention owing to their heavy annual output and extensive global flux. The updated epidemiological or experimental investigations have demonstrated the potential myocardial toxicity triggered by SiNPs, but the underlying mechanisms and long-lasting cardiac effects are still poorly understood. Here, a rat model of sub-chronic respiratory exposure to SiNPs was conducted, and the histopathological analysis and ultrastructural investigation of heart tissues were carried out.

Biomarkers for the adverse effects on respiratory system health associated with atmospheric particulate matter exposure.

Large amounts of epidemiological evidence have confirmed the atmospheric particulate matter (PM) exposure was positively correlated with the morbidity and mortality of respiratory diseases. Nevertheless, its pathogenesis remains incompletely understood, probably resulting from the activation of oxidative stress, inflammation, altered genetic and epigenetic modifications in the lung upon PM exposure. Currently, biomarker investigations have been widely used in epidemiological and toxicological studies, which may help in understanding the biologic mechanisms underlying PM-elicited adverse health outcomes.

Oxidative stress- and mitochondrial dysfunction-mediated cytotoxicity by silica nanoparticle in lung epithelial cells from metabolomic perspective.

Quantities of researches have demonstrated silica nanoparticles (SiNPs) exposure inevitably induced damage to respiratory system, nonetheless, knowledge of its toxicological behavior and metabolic interactions with the cellular machinery that determines the potentially deleterious outcomes are limited and poorly elucidated. Here, the metabolic responses of lung bronchial epithelial cells (BEAS-2B) under SiNPs exposure were investigated using ultra performance liquid chromatography-mass spectrum (UPLC-MS)-based metabolomics research. Results revealed that even with low cytotoxicity, SiNPs disturbed global metabolism.

Disturbed mitochondrial quality control involved in hepatocytotoxicity induced by silica nanoparticles.

The extensive application of silica nanoparticles (SiNPs) brings about inevitable occupational, environmental, and even iatrogenic exposure for human beings. The liver, which is rich in mitochondria, is one of the target organs of SiNPs, but the underlying mechanisms by which these nanoparticles (NPs) interact with liver mitochondria and affect their functions still remain unclear. In the present study, we examined silicon nanoparticle (SiNP)-induced mitochondrial dysfunction, and further revealed its negative effects on mitochondrial quality control (MQC) in the human liver cell line L-02, including mitochondrial dynamics, mitophagy and biogenesis.

PM triggered apoptosis in lung epithelial cells through the mitochondrial apoptotic way mediated by a ROS-DRP1-mitochondrial fission axis.

Epidemiological studies revealed a sharp increase in respiratory diseases attributed to PM. However, the underlying mechanisms remain unclear. Evidence suggested mitochondrion as a sensitive target upon the stimulus of PM, and the centrality in the pathological processes and clinical characterization of lung diseases.