Objective:This study aims to investigate the role of fatty acid-binding protein 4 (FABP4) in endothelial-to-mesenchymal transition (EndMT) during the formation of idiopathic pulmonary fibrosis (IPF) and its possible mechanism, and to evaluate the therapeutic potential ofFABP4 inhibitor BMS309403.Methods:A bleomycin (BLM)-induced mouse model of pulmonary fibrosis was established for in vivo experiments.hematoxylin-eosin(HE)and Masson staining were used to assess the histopathological changes and collagen deposition in lung tissue, while western blotting (WB) was used to assess EndMT-related protein expression in lung tissue.In vitro, human umbilical vein endothelial cells (HUVEC) were treated with transforming growth factor-β (TGF-β) to induce the EndMT model.After intervention with FABP4 protein or BMS309403, the expression levels of EndMT related genes and peroxisome proliferator-activated receptor γ (PPAR γ) were detected.Results:BLM-induced mice showed significant pulmonary fibrosis, inflammatory infiltration, and EndMT (upregulated expression of Fibronectin and α-SMA proteins expression, downregulated expression of VE cadherin and CD31 proteins), and BMS309403 treatment significantly alleviated these pathological changes.In vitro experiments confirmed that TGF-β could successfully induce EndMT in HUVECs, FABP4 enhanced the induction effect of TGF-β on EndMT, and BMS309403 could effectively reverse this effect.The co-treatment with TGF-β and FABP4 significantly inhibited the expression of PPARγ, BMS309403 significantly alleviated these changes.Conclusions:FABP4 may promote pulmonary fibrosis progression by facilitating EndMT through the PPARγ signaling pathway.FABP4 may serve as a promising therapeutic target for IPF.

Objective:This study aims to investigate the role of fatty acid-binding protein 4 (FABP4) in endothelial-to-mesenchymal transition (EndMT) during the formation of idiopathic pulmonary fibrosis (IPF) and its possible mechanism, and to evaluate the therapeutic potential ofFABP4 inhibitor BMS309403.Methods:A bleomycin (BLM)-induced mouse model of pulmonary fibrosis was established for in vivo experiments.hematoxylin-eosin(HE)and Masson staining were used to assess the histopathological changes and collagen deposition in lung tissue, while western blotting (WB) was used to assess EndMT-related protein expression in lung tissue.In vitro, human umbilical vein endothelial cells (HUVEC) were treated with transforming growth factor-β (TGF-β) to induce the EndMT model.After intervention with FABP4 protein or BMS309403, the expression levels of EndMT related genes and peroxisome proliferator-activated receptor γ (PPAR γ) were detected.Results:BLM-induced mice showed significant pulmonary fibrosis, inflammatory infiltration, and EndMT (upregulated expression of Fibronectin and α-SMA proteins expression, downregulated expression of VE cadherin and CD31 proteins), and BMS309403 treatment significantly alleviated these pathological changes.In vitro experiments confirmed that TGF-β could successfully induce EndMT in HUVECs, FABP4 enhanced the induction effect of TGF-β on EndMT, and BMS309403 could effectively reverse this effect.The co-treatment with TGF-β and FABP4 significantly inhibited the expression of PPARγ, BMS309403 significantly alleviated these changes.Conclusions:FABP4 may promote pulmonary fibrosis progression by facilitating EndMT through the PPARγ signaling pathway.FABP4 may serve as a promising therapeutic target for IPF.

Objective This study aimed to explore the relationships between residential greenness and cardiometabolic risk factors among rural adults in Xinjiang Uygur Autonomous Region(Xinjiang)and thus provide a theoretical basis and data support for improving the health of residents in this region. Methods We recruited 9,723 adult rural residents from the 51st Regiment of the Third Division of the Xinjiang Production and Construction Corps in September 2016.The normalized difference vegetation index(NDVI)was used to estimate residential greenness.The generalized linear mixed model(GLMM)was used to examine the association between residential greenness and cardiometabolic risk factors. Results Higher residential greenness was associated with lower cardiometabolic risk factor prevalence.After adjustments were made for age,sex,education,and marital status,for each interquartile range(IQR)increase of NDVI500-m,the risk of hypertension was reduced by 10.3%(OR=0.897,95%CI=0.836-0.962),the risk of obesity by 20.5%(OR=0.795,95%CI=0.695-0.910),the risk of type 2 diabetes by 15.1%(OR=0.849,95%CI=0.740-0.974),and the risk of dyslipidemia by 10.5%(OR=0.895,95%CI=0.825-0.971).Risk factor aggregation was reduced by 20.4%(OR=0.796,95%CI=0.716-0.885)for the same.Stratified analysis showed that NDVI500-m was associated more strongly with hypertension,dyslipidemia,and risk factor aggregation among male participants.The association of NDVI500-m with type 2 diabetes was stronger among participants with a higher education level.PM10 and physical activity mediated 1.9%-9.2%of the associations between NDVI500-m and obesity,dyslipidemia,and risk factor aggregation. Conclusion Higher residential greenness has a protective effect against cardiometabolic risk factors among rural residents in Xinjiang.Increasing the area of green space around residences is an effective measure to reduce the burden of cardiometabolic-related diseases among rural residents in Xinjiang.