2. Academic Validation
  3. Silicon carbide nanoparticles induce pulmonary fibrosis by promoting macrophage apoptosis through parkin-mediated mitophagy disruption and the intervention effect of emodin

Silicon carbide nanoparticles induce pulmonary fibrosis by promoting macrophage apoptosis through parkin-mediated mitophagy disruption and the intervention effect of emodin

  • J Hazard Mater. 2026 Apr 1:507:141765. doi: 10.1016/j.jhazmat.2026.141765.
Sufang Wu 1,  Xianglong Wu 1,  Nuo Xu 1,  Ze Li 1,  Yang Dong 1,  Chenxing Zhang 2,  Qian Liu 1,  Huang Chen 3,  Lele Liu 1,  Yanxin Hu 1,  Gancen Zhang 2,  Yunru Liu 4,  Jin Xu 5,  Aihua Gu 6
Affiliations

Affiliations

  • 1 State Key Laboratory of Reproductive Medicine and Offspring Health, School of Public Health, Nanjing Medical University, Nanjing 211166, China; Jiangsu Environmental Health Risk Assessment Engineering Research Center, Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, Nanjing Medical University, Nanjing 211166, China.
  • 2 The First School of Clinical Medicine, Nanjing Medical University, Nanjing, China.
  • 3 State Key Laboratory of Reproductive Medicine and Offspring Health, School of Public Health, Nanjing Medical University, Nanjing 211166, China; Jiangsu Environmental Health Risk Assessment Engineering Research Center, Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, Nanjing Medical University, Nanjing 211166, China; The First Affiliated Hospital of Bengbu Medical University, Bengbu 233000, China.
  • 4 School of Public Health, Hainan Medical University, Haikou 571199, China.
  • 5 State Key Laboratory of Reproductive Medicine and Offspring Health, School of Public Health, Nanjing Medical University, Nanjing 211166, China; Jiangsu Environmental Health Risk Assessment Engineering Research Center, Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, Nanjing Medical University, Nanjing 211166, China; Key Laboratory of Public Health Safety and Emergency Prevention and Control Technology of Higher Education Institutions in Jiangsu Province, Nanjing Medical University, Nanjing 211166, China. Electronic address: [email protected].
  • 6 State Key Laboratory of Reproductive Medicine and Offspring Health, School of Public Health, Nanjing Medical University, Nanjing 211166, China; Jiangsu Environmental Health Risk Assessment Engineering Research Center, Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, Nanjing Medical University, Nanjing 211166, China. Electronic address: [email protected].
PMID: 41864028 DOI: 10.1016/j.jhazmat.2026.141765
Abstract

Silicon carbide nanoparticles (SiC-NPs), an emerging class of nanomaterials, have garnered extensive applications in industrial and biomedical fields. The escalating use of SiC-NPs engenders substantial concerns regarding the potential biosafety implications. Previous studies indicate the association between silicon carbide exposure and elevated incidence of pulmonary fibrosis. However, the underlying mechanisms remain insufficiently elucidated. In this study, we investigated the role of SiC-NPs in pulmonary fibrosis development, employing THP-1-derived macrophages (THP-M) for in vitro experimentation and C57BL/6 mice for in vivo analyses. Our study demonstrated that exposure to SiC-NPs led to the production of Reactive Oxygen Species (ROS) and mitochondrial damage in macrophages. This sequence of events impaired Mitophagy and subsequently triggered macrophage Apoptosis, ultimately contributing to the pathogenesis of pulmonary fibrosis. Mechanistically, we elucidated that SiC-NPs promoted the ubiquitin-mediated degradation of Parkin, resulting in dysregulated Mitophagy. Furthermore, we revealed that emodin treatment mitigated SiC-NPs-induced pulmonary fibrosis by restoring Parkin expression. Our study provides novel insights into the detrimental effects and underlying mechanisms of SiC-NPs in pulmonary fibrosis, as well as highlighting the therapeutic potential of emodin.

Keywords

Emodin; Macrophage; Mitophagy; Pulmonary fibrosis; Silicon carbide nanoparticles.

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