Shoude Jin
Abstract
Chronic obstructive pulmonary disease (COPD) is a complex multifactorial disease involving both genetic and environmental factors and is one of the leading causes of death worldwide. Although considerable improvements have been made in controlling environmental factors, the morbidity and mortality of COPD continues to increase. In recent years, we have focused on the genetic factors contributing to COPD, starting with the ABHD2 mutations. We found that the ABHD2 gene trap mice spontaneously developed into emphysema. These results strongly suggest the role of ABHD2 mutations in the development of COPD, but the exact mechanisms and whether ABHD2 mutations can be used as warning markers for COPD remain largely unknown. Based on the results according to which ABHD2 is expressed in smooth muscle cells of the respiratory tract, in the next research project, we propose to test our hypothesis that ABHD2 regulates apoptosis of alveolar epithelial type cells at the cellular level and animal and elucidate the effects of specific mutations of ABHD2 on COPD, and use ovalbumin to stimulate ABHD2-deficient mice with a genetic background of COPD and trigger asthma attacks. The goal is to clarify the function and structure of changes in smooth muscle cells in the airways to promote inflammation and remodeling, making it easier for COPD to develop ACOS in mice deficient in Abhd2. Finally, we hope to provide a theoretical basis and potential key drug targets for early detection and early intervention for people at high risk for COPD and identify potential key drug targets and provide new strategies for precise clinical treatment. The protein 2 gene containing the human α / β hydrolase domain (ABHD2) plays an essential role in pulmonary emphysema, a major subset of the clinical entity known as chronic obstructive pulmonary disease (COPD). Here, we evaluated the genetic variation of the ABHD2 gene in a Han Chinese population of 286 COPD patients and 326 control subjects. The rs12442260 CT / CC genotype has been associated with COPD (P