Kim Ha Ryong, Shin Da Young, Chung Kyu Hyuck
College of Pharmacy, Daegu Catholic University, Gyeongsan, Gyeongsangbuk-do 38430, Republic of Korea.
School of Pharmacy, Sungkyunkwan University, Suwon, Gyeonggi-do 16419, Republic of Korea.
Environ Health Toxicol. 2018 Sep;33(3):e2018014-0. doi: 10.5620/eht.e2018014. Epub 2018 Sep 28.
Several studies showed that the inflammatory and fibrotic responses induced by polyhexamethylene guanidine phosphate (PHMG-p) were similar to those observed for idiopathic pulmonary fibrosis in South Korea in 2011. "Omic" technologies can be used to understand the mechanisms underlying chemical-induced diseases. Studies to determine the toxicity of chemicals may facilitate understanding of the mechanisms underlying the development of pulmonary fibrosis at a molecular level; thus, such studies may provide information about the toxic characteristics of various substances. In this review, we have outlined the cellular and molecular mechanisms underlying idiopathic pulmonary fibrosis and described pulmonary fibrosis induced by various chemicals, including bleomycin, paraquat, and PHMG-p, based on the results of studies performed to date.
多项研究表明,聚六亚甲基胍磷酸盐(PHMG-p)诱导的炎症和纤维化反应与2011年韩国特发性肺纤维化所观察到的反应相似。“组学”技术可用于了解化学物质诱发疾病的潜在机制。确定化学物质毒性的研究可能有助于在分子水平上理解肺纤维化发展的潜在机制;因此,此类研究可能提供有关各种物质毒性特征的信息。在本综述中,我们概述了特发性肺纤维化的细胞和分子机制,并根据迄今为止进行的研究结果,描述了包括博来霉素、百草枯和PHMG-p在内的各种化学物质诱发的肺纤维化。