Analyzing biological and molecular characteristics and genomic damage induced by exposure to asbestos

Asbestos is one of the most important occupational carcinogens. Currently, about 125 million people worldwide are exposed to asbestos in the workplace. According to global estimates, at least 107,000 people die each year from lung cancer, mesothelioma, and asbestosis as a result of occupational exposure to asbestos. The high pathogenicity of this material is currently known, being associated with the development of pulmonary diseases, of which lung cancer is the main cause of death due to exposure to this mineral. Pulmonary diseases related to asbestos are a common clinical problem and a major health concern worldwide. Extensive research has identified many important pathogenic mechanisms; however, the precise molecular mechanisms involved, and the generated genomic damage that lead to the development of these diseases, are not completely understood. The modes of action that underlie this type of disease seem to differ depending on the type of fiber, lung clearance, and genetics. This evidences the need to increase our knowledge about these effects on human health. This review focuses on the characteristics of asbestos and the cellular and genomic damage generated in humans via exposure. © 2019 Zhang et al.

• Fecha de publicación: 2019
• Institución: Universidad del Rosario
• Repositorio: Repositorio EdocUR - U. Rosario
• Idioma: eng
• OAI Identifier: oai:repository.urosario.edu.co:10336/23635
• Acceso en línea: https://doi.org/10.2147/CMAR.S205723; https://repository.urosario.edu.co/handle/10336/23635
• Palabra clave: Anaplastic lymphoma kinase; Aquaporin 1; Asbestos; Cyclin dependent kinase inhibitor 2a; Cyclin dependent kinase inhibitor 2b; Epidermal growth factor receptor; Fibronectin; Fibulin; Fibulin 3; Fragile histidine triad protein; High mobility group b1 protein; Immunoglobulin enhancer binding protein; Interleukin 6; Interleukin 8; Mesothelin; Messenger rna; Mitogen activated protein kinase; Mitogen activated protein kinase 1; Mitogen activated protein kinase 3; Osteopontin; Reactive nitrogen species; Reactive oxygen metabolite; Soluble mesothelin related protein; Transcription factor ap 1; Unclassified drug; Alk gene; Angiogenesis; Asbestosis; Bap1 gene; Cancer risk; Cause of death; Cdkn2a gene; Cdkn2b gene; Chromosome damage; Cul1 gene; Dna damage; Fhit gene; Fibrogenesis; Gene; Gene mutation; Gene rearrangement; Genetic damage; Genetic predisposition; Human; Lung alveolus cell type 2; Lung alveolus macrophage; Lung cancer; Mapk signaling; Mesothelioma; Met gene; Nf2 gene; Nonhuman; Occupational exposure; Oxidative stress; Pathogenicity; Protein phosphorylation; Review; Smoking; Workplace; Cancer; Cellular damage; Genomic damage; Occupational exposure
• License: Abierto (Texto Completo)