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Mitochondrial dysfunction-associated alveolar epithelial senescence is involved in CdCl2-induced COPD-like lung injury.
Peng, Kun; Yao, Ya-Xin; Lu, Xue; Wang, Wen-Jing; Zhang, Yi-Hao; Zhao, Hui; Wang, Hua; Xu, De-Xiang; Tan, Zhu-Xia.
Afiliación
  • Peng K; Department of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Anhui Medical University, Hefei, China.
  • Yao YX; Department of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Anhui Medical University, Hefei, China.
  • Lu X; Department of Toxicology, School of Public Health, Anhui Medical University, Hefei, China.
  • Wang WJ; Department of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Anhui Medical University, Hefei, China.
  • Zhang YH; Department of Toxicology, School of Public Health, Anhui Medical University, Hefei, China.
  • Zhao H; Department of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Anhui Medical University, Hefei, China.
  • Wang H; Department of Toxicology, School of Public Health, Anhui Medical University, Hefei, China.
  • Xu DX; Department of Toxicology, School of Public Health, Anhui Medical University, Hefei, China. Electronic address: xudex@126.com.
  • Tan ZX; Department of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Anhui Medical University, Hefei, China. Electronic address: tanzhuxia@126.com.
J Hazard Mater ; 476: 135103, 2024 Sep 05.
Article en En | MEDLINE | ID: mdl-38972203
ABSTRACT
An earlier study found that respiratory cadmium chloride (CdCl2) exposure caused COPD-like lung injury. This study aimed to explore whether mitochondrial dysfunction-mediated alveolar epithelial senescence is involved in CdCl2-induced COPD-like lung injury. Adult C57BL/6 mice were exposed to CdCl2 (10 mg/L) aerosol for six months. Beta-galactosidase-positive cells, p21 and p16 were increased in CdCl2-exposed mouse lungs. The in vitro experiments showed that γ-H2AX was elevated in CdCl2-exposed alveolar epithelial cells. The cGAS-STING pathway was activated in CdCl2-exposed alveolar epithelial cells and mouse lungs. Cxcl1, Cxcl9, Il-10, Il-1ß and Mmp2, several senescence-associated secretory phenotypes (SASP), were upregulated in CdCl2-exposed alveolar epithelial cells. Mechanistically, CdCl2 exposure caused SIRT3 reduction and mitochondrial dysfunction in mouse lungs and alveolar epithelial cells. The in vitro experiment found that Sirt3 overexpression attenuated CdCl2-induced alveolar epithelial senescence and SASP. The in vivo experiments showed that Sirt3 gene knockout exacerbated CdCl2-induced alveolar epithelial senescence, alveolar structure damage, airway inflammation and pulmonary function decline. NMN, an NAD+ precursor, attenuated CdCl2-induced alveolar epithelial senescence and SASP in mouse lungs. Moreover, NMN supplementation prevented CdCl2-induced COPD-like alveolar structure damage, epithelial-mesenchymal transition and pulmonary function decline. These results suggest that mitochondrial dysfunction-associated alveolar epithelial senescence is involved in CdCl2-induced COPD-like lung injury.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Senescencia Celular / Enfermedad Pulmonar Obstructiva Crónica / Ratones Endogámicos C57BL / Mitocondrias Límite: Animals Idioma: En Revista: J Hazard Mater Asunto de la revista: SAUDE AMBIENTAL Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Países Bajos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Senescencia Celular / Enfermedad Pulmonar Obstructiva Crónica / Ratones Endogámicos C57BL / Mitocondrias Límite: Animals Idioma: En Revista: J Hazard Mater Asunto de la revista: SAUDE AMBIENTAL Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Países Bajos