Article
Nanoscience & Nanotechnology
Dong Kyu Yoo, Ho Chul Woo, Sung Hwa Jhung
Summary: The study demonstrates that modifying highly porous metal-organic frameworks and adding ionic salts can significantly enhance the filtration efficiency of particulate matters in the air. This method not only improves filter performance, but also addresses the challenge of removing large particles with sizes in the micron range using materials with nanometer-scale or smaller pores.
ACS APPLIED MATERIALS & INTERFACES
(2021)
Article
Medicine, Research & Experimental
Omaima A. Ahmedy, Marwa W. Kamel, Dalia M. Abouelfadl, Marwa E. Shabana, Rabab H. Sayed
Summary: This study discovered the protective effects of berberine in bleomycin-induced pulmonary fibrosis in mice, and its mechanism involved the activation of adenosine A2a receptor and suppression of SDF-1/CXCR4 signaling pathway. Berberine improved lung fibrosis by modulating the purinergic system, inhibiting epithelial mesenchymal transition, and effectively suppressing inflammation and oxidative stress.
Article
Biochemistry & Molecular Biology
Claudia De Vitis, Michela D'Ascanio, Andrea Sacconi, Dario Pizzirusso, Valentina Salvati, Massimiliano Mancini, Giorgia Scafetta, Roberto Cirombella, Francesca Ascenzi, Sara Bruschini, Antonella Esposito, Silvia Castelli, Claudia Salvucci, Leonardo Teodonio, Bruno Sposato, Angela Catizone, Arianna Di Napoli, Andrea Vecchione, Gennaro Ciliberto, Salvatore Sciacchitano, Alberto Ricci, Rita Mancini
Summary: The study revealed that the B4GALT1 gene is overexpressed in IPF patients and human cell cultures, indicating it could serve as a potential novel marker for this disease.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Medicine, Research & Experimental
Wenping Liu, Xiao Han, Qing Li, Linqian Sun, Jibo Wang
Summary: This study found that IGU has therapeutic effects on pulmonary fibrosis by inhibiting the EMT process and NLRP3 inflammasome activation, reducing ROS production. This may provide new possibilities for the application of IGU in the treatment of interstitial pulmonary fibrosis.
BIOMEDICINE & PHARMACOTHERAPY
(2022)
Article
Medicine, Research & Experimental
Yan Gao, Zhaoyun Yang, Kang He, Zeyu Wang, Tingyu Zhang, Jiang Yi, Lijing Zhao
Summary: This study found that exercise has anti-inflammatory and antioxidant effects on pulmonary fibrosis induced by paraquat, reducing the infiltration of inflammatory cells and fibrotic lesions. Furthermore, exercise also increased the expression of antioxidative distress proteins, improved the degree of epithelial-mesenchymal transition in alveolar epithelial cells, and ultimately alleviated paraquat-induced pulmonary fibrosis.
Review
Biochemistry & Molecular Biology
Ezgi Sari, Chao He, Camilla Margaroli
Summary: Idiopathic pulmonary fibrosis (IPF) is a fatal lung disease with unclear molecular mechanisms and limited effective treatments. Macrophages play a crucial role in IPF by potentially contributing to fibrosis while also having the potential for amelioration.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Environmental Sciences
Bayu Hadi Permana, Paitip Thiravetyan, Chairat Treesubsuntorn
Summary: This study examines the removal efficiency of particulate matters (PMs) and volatile organic compounds (VOCs) using a botanical biofilter. Results show that the removal efficiency depends on the distance and airflow pattern. The highest elimination of PMs is at 240 cm and 315 cm, while VOCs removal is high at 100 cm.
Review
Biochemistry & Molecular Biology
Ana Ruth Cadena-Suarez, Hilda Arely Hernandez-Hernandez, Noe Alvarado-Vasquez, Claudia Rangel-Escareno, Bettina Sommer, Maria Cristina Negrete-Garcia
Summary: Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive disease with high mortality and unclear etiology. miRNAs may play a role in the development of IPF by regulating signaling pathways involved in the disease. Understanding the molecular mechanisms associated with miRNAs and IPF could potentially lead to new therapeutic targets for this severe lung disease.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Engineering, Multidisciplinary
Keiichiro Yoshida
Summary: A novel electrostatic precipitator was developed to collect and decompose soot in exhaust gas. The uneven surface potential was found to be the key factor in particle collection.
IEEE TRANSACTIONS ON INDUSTRY APPLICATIONS
(2022)
Article
Immunology
Shuangling Li, Shaoyan Gao, Qiuyan Jiang, Qing Liang, Jiaoyan Luan, Ruiqin Zhang, Fangxia Zhang, Hao Ruan, Xiaohe Li, Xiaoping Li, Honggang Zhou, Cheng Yang
Summary: The study found that clevudine is capable of suppressing profibrotic phenotype of M2 macrophages while enhancing anti-fibrotic phenotype by inhibiting the PI3K/Akt signaling pathway. This leads to alleviation of myofibroblast activation and epithelial-to-mesenchymal transition induced by M2, resulting in a decline of collagen deposition and pro-fibrotic cytokines secretion, as well as a recovery of pulmonary functions in vivo. Additionally, less infiltration of M2 macrophages was observed in clevudine treated mice, indicating a potential anti-fibrotic effect of clevudine by regulating macrophage polarization.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2021)
Article
Environmental Sciences
Naresh Singh, Naveen Arora
Summary: The study found that exposure to diesel exhaust in mice led to lung injury and pulmonary fibrosis, as evidenced by impaired lung function, cellular infiltration, inflammation, thickening of the alveolar wall, and tissue remodeling. The involvement of the TGF-beta/SMAD3 pathway and activation of EMT in diesel exhaust-exposed mice was demonstrated.
SCIENCE OF THE TOTAL ENVIRONMENT
(2022)
Article
Pharmacology & Pharmacy
Qing Li, Meng-Sheng Deng, Ren-Tao Wang, Hao Luo, Yuan-Yuan Luo, Dong-Dong Zhang, Kui-Jun Chen, Xiao-Fu Cao, Guang-Ming Yang, Tie-Mei Zhao, Bo Xu, Cheng-Xiong Xu, Jian-Min Wang
Summary: This study demonstrated that PD-L1 is upregulated in fibrotic lung tissues and sera of IPF patients. PD-L1 upregulation stimulates EMT (Epithelial-Mesenchymal Transition) and fibrosis-like morphology changes by inhibiting vimentin ubiquitination and increasing vimentin levels in alveolar epithelial cells, contributing to pulmonary fibrosis.
PHARMACOLOGICAL RESEARCH
(2023)
Article
Pharmacology & Pharmacy
Qiuyun Wu, Wenwen Gui, Biyang Jiao, Lei Han, Feng Wang
Summary: In this study, a mouse model of pulmonary fibrosis was established by intratracheal instillation of silica particles, and it was found that miR-138 targets ZEB2 to inhibit the process of epithelial-mesenchymal transition (EMT) and alleviate the development of pulmonary fibrosis. The overexpression of miR-138 significantly reduced the expression of ZEB2 and reversed the effects of miR-138 inhibitor on the migration ability of epithelial cells. MiR-138 may serve as a potential target for the treatment of pulmonary fibrosis.
Article
Immunology
Yang Miao, Xiaohe Li, Yue Yang, Jianwei Zhang, Li Chen, Qianyi Zhang, Wenqi Li, Ying Liu, Xianfeng Zhang, Ruimin Gu, Cheng Yang
Summary: In this study, it was found that Entrectinib effectively inhibits the development of pulmonary fibrosis by blocking TGF-β1 signaling, both in vitro and in vivo.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Yunzhang Wu, Yongchao Qi, Zhibing Qiu, Wen Chen
Summary: The study demonstrates that CARMA3 plays a crucial role in the pathogenesis of bleomycin-induced pulmonary fibrosis, potentially offering a target for therapeutic intervention by mitigating inflammation, collagen deposition, and alveolar epithelial cell damage.
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
(2021)
Article
Cell Biology
Ming-Hsien Chiang, Chan-Jung Liang, Lung-Chun Lin, Yi-Fan Yang, Ching-Chang Huang, Ying-Hsien Chen, Hsien-Li Kao, Yu-Chen Chen, Shin-Rong Ke, Chiang-Wen Lee, Mao-Shin Lin, Yuh-Lien Chen
JOURNAL OF CELLULAR PHYSIOLOGY
(2020)
Article
Cell Biology
Yu-Chen Chen, Hsin-Ching Sung, Tzu-Yi Chuang, Tsai-Chun Lai, Tzu-Lin Lee, Chiang-Wen Lee, I-Ta Lee, Yuh-Lien Chen
Summary: This study elucidated the mechanisms by which Vitamin D reduces the expression of adhesion molecules in models of airway inflammation. Vitamin D may serve as a novel therapeutic agent for targeting epithelial activation in lung inflammation.
CELL BIOLOGY AND TOXICOLOGY
(2022)
Article
Dentistry, Oral Surgery & Medicine
Thi Thuy Tien Vo, Yinshen Wee, Yuh-Lien Chen, Hsin-Chung Cheng, Vo Phuoc Tuan, I-Ta Lee
Summary: Surfactin exhibits anti-inflammatory effects against PM-induced oral inflammatory responses in HGFs by disrupting the TLR2 and TLR4/MyD88/NADPH oxidase/ROS/PI3K/Akt/NF-kappa B pathway, as demonstrated in both cell culture and mouse models.
JOURNAL OF PERIODONTAL RESEARCH
(2021)
Article
Dentistry, Oral Surgery & Medicine
Thi Thuy Tien Vo, Yinshen Wee, Hsin-Chung Cheng, Ching-Zong Wu, Yuh-Lien Chen, Vo Phuoc Tuan, Ju-Fang Liu, Wei-Ning Lin, I-Ta Lee
Summary: This study investigated the anticancer effects and underlying mechanisms of surfactin on human oral squamous cell carcinoma (OSCC). The results showed that surfactin could induce apoptosis, autophagy, and cell cycle arrest through different signaling pathways. The study suggests that surfactin may serve as a multifaceted anticancer agent for OSCC.
Article
Cell Biology
Thi Thuy Tien Vo, Chien-Yi Hsu, Yinshen Wee, Yuh-Lien Chen, Hsin-Chung Cheng, Ching-Zong Wu, Wei-Ning Lin, I-Ta Lee
Summary: CORM-2 treatment showed multiple beneficial effects on inflammatory responses induced by PM exposure, providing therapeutic value in inflammatory diseases of the cardiovascular system.
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
(2021)
Article
Pharmacology & Pharmacy
Chien-Yi Hsu, Thi Thuy Tien Vo, Chiang-Wen Lee, Yuh-Lien Chen, Wei-Ning Lin, Hsin-Chung Cheng, Quang Chanh Vo, I-Ta Lee
Summary: The study found that CORM-2 can inhibit Ang II-induced inflammatory responses and alleviate the proliferation, migration, and inflammation of vascular smooth muscle cells. In addition, CORM-2 also reduces monocyte adhesion and cell migration by inhibiting specific molecules and signaling pathways. The results of the study also suggest that CORM-2 can reverse Ang II-induced IL-6 overexpression by activating Nrf2 and HO-1.
BIOCHEMICAL PHARMACOLOGY
(2022)
Article
Toxicology
Tsai-Chun Lai, Yu-Chen Chen, Hui-Hua Cheng, Tzu-Lin Lee, Jaw-Shiun Tsai, I-Ta Lee, Kuo-Ti Peng, Chiang-Wen Lee, Lee-Fen Hsu, Yuh-Lien Chen
Summary: This study found that simultaneous exposure to PM2.5 and high glucose has significant harmful effects on endothelial cells, potentially exacerbating endothelial damage. Vitamin D can alleviate these effects.
PARTICLE AND FIBRE TOXICOLOGY
(2022)
Article
Multidisciplinary Sciences
Yi-Hsuan Kuo, Tsai-Chun Lai, Chia-Hsin Chang, Han-Ching Hsieh, Feng-Ming Yang, Meng-Chun Hu
Summary: DRB treatment inhibits proliferation and induces apoptosis in breast cancer cells by downregulating Mcl-1 protein. Co-treatment with AKT inhibitor or proteasome inhibitor enhances the apoptotic effect of DRB in breast cancer cells.
SCIENTIFIC REPORTS
(2023)
Article
Nanoscience & Nanotechnology
Tsai-Chun Lai, Chiang-Wen Lee, Mei-Hsiang Hsu, Yu-Chen Chen, Shu-Rung Lin, Shu-Wha Lin, Tzu-Lin Lee, Shin-Yu Lin, Shu-Hao Hsu, Jaw-Shiun Tsai, Yuh-Lien Chen
Summary: This study elucidated the mechanisms of how high glucose (HG) and particulate matter (PM) induce endothelial inflammation, as well as the protective effect of nanocurcumin (NCur) in alleviating inflammation.
INTERNATIONAL JOURNAL OF NANOMEDICINE
(2023)
Article
Oncology
Thi Thuy Tien Vo, Ju-Fang Liu, Ching-Zong Wu, Wei-Ning Lin, Yuh-Lien Chen, I-Ta Lee
Article
Oncology
Thi Thuy Tien Vo, Chiang-Wen Lee, Ching-Zong Wu, Ju-Fang Liu, Wei-Ning Lin, Yuh-Lien Chen, Lee-Fen Hsu, Ming-Horng Tsai, I-Ta Lee
Article
Medicine, Research & Experimental
Tzu-Lin Lee, Tsai-Chun Lai, Shu-Rung Lin, Shu-Wha Lin, Yu-Chen Chen, Chi-Ming Pu, I-Ta Lee, Jaw-Shiun Tsai, Chiang-Wen Lee, Yuh-Lien Chen
Summary: The study demonstrates that ADSC-CM significantly reduces injury and fibrosis in I/R-treated hearts and H/R-treated cardiomyocytes, while decreasing expression of related proteins and promoting cell survival through the miR-221/222/p38/NF-kappa B pathway.