Article
Pharmacology & Pharmacy
Huimin Ji, Hongliang Dong, Yuejiao Lan, Yuqian Bi, Xuan Gu, Yongyue Han, Chongyang Yang, Minghan Cheng, Jian Gao
Summary: This study demonstrates that Metformin attenuates the progression of lung fibrosis by inhibiting the activation of fibroblasts through down-regulating S100A4 expression and STAT3 phosphorylation. It provides a potential clinical strategy for preventing pulmonary fibrosis.
FRONTIERS IN PHARMACOLOGY
(2023)
Article
Medicine, Research & Experimental
Demin Cheng, Qi Xu, Yue Wang, Guanru Li, Wenqing Sun, Dongyu Ma, Siyun Zhou, Yi Liu, Lei Han, Chunhui Ni
Summary: The study found that metformin significantly reduced lung inflammation and fibrosis in silica-induced lung fibrosis model. Metformin reversed silica-induced cell toxicity, oxidative stress, and epithelial-mesenchymal transition process in epithelial cells and macrophages, as well as alleviated TGF-beta 1-stimulated fibroblast activation in lung fibroblasts via an AMPK-dependent pathway.
JOURNAL OF TRANSLATIONAL MEDICINE
(2021)
Article
Pharmacology & Pharmacy
Xuan Gu, Yong-Yue Han, Chong-Yang Yang, Hui-Min Ji, Yue-Jiao Lan, Yu-Qian Bi, Cheng Zheng, Jiao Qu, Ming-Han Cheng, Jian Gao
Summary: In this study, the relationship between AMPK and FOXM1 in fibroblast proliferation-mediated pulmonary fibrosis (PF) was investigated. The results showed that activation of AMPK by metformin down-regulated FOXM1 and alleviated PF in mouse models, while inhibition of AMPK enhanced fibroblast proliferation. This study provides new insights into potential treatment approaches for PF involving the regulation of FOXM1 by AMPK.
PHARMACOLOGICAL RESEARCH
(2021)
Article
Biochemistry & Molecular Biology
Tatsuro Ogawa, Shigeyuki Shichino, Satoshi Ueha, Shuhei Ogawa, Kouji Matsushima
Summary: C1q, a complement protein, plays an important role in pulmonary fibrosis. This study found that inhibiting C1q could improve pulmonary fibrosis, while administration of C1q induced fibrotic changes. Further experiments revealed that C1q activated fibroblasts and type 2 alveolar epithelial cells, leading to the expression of fibrosis-related genes. These findings suggest that C1q may be a potential therapeutic target for pulmonary fibrosis.
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
(2022)
Article
Biochemistry & Molecular Biology
Megane Lebel, Dominic O. Cliche, Martine Charbonneau, Damien Adam, Emmanuelle Brochiero, Claire M. Dubois, Andre M. Cantin
Summary: Idiopathic pulmonary fibrosis (IPF) is characterized by abnormal fibroblast accumulation in the lung leading to compromised lung function. This study investigated the mechanisms of interstitial invasion and remodeling by lung fibroblasts in IPF and found increased invadosome formation. Additionally, two drugs approved for treating IPF, nintedanib and pirfenidone, were found to suppress invadosome formation in IPF lung fibroblasts.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Biochemistry & Molecular Biology
Aurelien Justet, Mada Ghanem, Tiara Boghanim, Mouna Hachem, Eirini Vasarmidi, Madeleine Jaillet, Aurelie Vadel, Audrey Joannes, Pierre Mordant, Philippe Bonniaud, Martin Kolb, Lei Ling, Aurelie Cazes, Herve Mal, Arnaud Mailleux, Bruno Crestani
Summary: This study identifies FGF19 as an antifibrotic molecule with potential therapeutic interest in fibrotic lung disorders. In vivo and in vitro experiments demonstrate that FGF19 can decrease lung fibrosis and fibrotic markers, modulate apoptosis of lung epithelial cells, and prevent myofibroblast differentiation.
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Dimitrios Kalafatis, Anna Loefdahl, Per Naesman, Goeran Dellgren, Asa M. Wheelock, Linda Elowsson Rendin, Magnus Skoeld, Gunilla Westergren-Thorsson
Summary: This study utilized a novel ex vivo model to investigate the association between protein changes in serum of patients with idiopathic pulmonary fibrosis (IPF) and disease severity and treatment response. The findings support the applicability of the model in studying IPF mechanisms and provide additional evidence for established and potentially new biomarkers in IPF.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Biochemistry & Molecular Biology
Yu Fujita, Shota Fujimoto, Atsushi Miyamoto, Reika Kaneko, Tsukasa Kadota, Naoaki Watanabe, Ryusuke Kizawa, Hironori Kawamoto, Junko Watanabe, Hirofumi Utsumi, Hiroshi Wakui, Shunsuke Minagawa, Jun Araya, Takashi Ohtsuka, Takahiro Ochiya, Kazuyoshi Kuwano
Summary: In this study, researchers found that extracellular vesicles (EVs) derived from lung fibroblasts (LFs) of patients with idiopathic pulmonary fibrosis (IPF) have an enrichment of miR-19a. These EVs contribute to the progression and poor prognosis of non-small cell lung cancer (NSCLC) by regulating c-Myc activation through ZMYND11. This study provides mechanistic insights into lung cancer progression in the IPF microenvironment.
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
(2023)
Article
Biochemistry & Molecular Biology
Laura Vera, Paula Garcia-Olloqui, Eva Petri, Ana Cristina Vinado, Pablo S. Valera, Zurine Blasco-Iturri, Isabel A. Calvo, Itziar Cenzano, Clemens Ruppert, Javier J. Zulueta, Felipe Prosper, Borja Saez, Ana Pardo-Saganta
Summary: The study highlights the crucial role of Notch3 in lung fibrosis, with Notch3 deficiency offering protection by reducing collagen deposition, decreasing the number of myofibroblasts, and improving lung function. This discovery uncovers a novel mechanism in lung fibrogenesis and suggests a potential new therapeutic approach for targeting pulmonary fibrosis.
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
(2021)
Article
Pharmacology & Pharmacy
Qing Liang, Yanhua Chang, Jing Liu, Yan Yu, Wancheng Qiu, Jiajia Li, Xu Yang, Guangchun Sun
Summary: The study identified P-Rex1 as a key molecule involved in TGF-beta 1-induced pulmonary fibrosis, with potential as a therapeutic target for the condition. Through knockdown and overexpression experiments, P-Rex1 was found to play a role in lung fibroblast migration and fibrogenic processes by targeting the TGF-beta type II receptor. RNA-seq analysis confirmed the involvement of P-Rex1 in cell migration and its modulation in TGF-beta 1 signaling.
FRONTIERS IN PHARMACOLOGY
(2021)
Article
Biotechnology & Applied Microbiology
Huaman Liu, Xinyue Zhang, Yumeng Shao, Xuehong Lin, Feng Dong, Xue Liu
Summary: Danshensu (DSS) has shown anti-fibrotic effects in heart and liver, and this study demonstrated its potential therapeutic role in pulmonary fibrosis by inhibiting lung fibroblast proliferation, migration, and differentiation through suppressing the MEK/ERK signaling pathway.
Article
Cell Biology
Xia Guo, Oluwaseun Adeyanju, Christudas Sunil, Venkatakirankumar Mandlem, Ayobami Olajuyin, Steven Huang, Shi-You Chen, Steven Idell, Torry A. Tucker, Guoqing Qian
Summary: DOCK2 plays a crucial role in pulmonary fibrosis by modulating FMT, with its upregulation dependent on TGF-beta induction and Smad3, ERK pathways, and contributing to the changes in lung fibroblast phenotypes.
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
(2022)
Article
Immunology
Siavash Bolourani, Ezgi Sari, Max Brenner, Ping Wang
Summary: The study demonstrates that eCIRP induces an inflammatory phenotype in pulmonary fibroblasts in a TLR4-dependent manner and is associated with bleomycin-induced pulmonary fibrosis.
FRONTIERS IN IMMUNOLOGY
(2021)
Article
Toxicology
Ji-Ming Sha, Ren-Quan Zhang, Xian-Chen Wang, Yang Zhou, Kai Song, He Sun, Bin Tu, Hui Tao
Summary: This study investigates the role of the epigenetic reader MeCP2 and its target WIF1 in pulmonary fibrosis. The results suggest that upregulation of MeCP2 and downregulation of WIF1 are associated with pulmonary fibrosis. Silencing of MeCP2 can rescue WIF1 expression and inhibit lung fibroblast activation. These findings highlight the importance of MeCP2 in the regulation of pulmonary fibrosis.
TOXICOLOGY LETTERS
(2023)
Review
Multidisciplinary Sciences
Xinxin Zhang, Xiaoni Shi, Feiyan Xie, Yaping Liu, Xinyan Wei, Yu Cai, Jie Chao
Summary: Lung fibroblasts are crucial in pulmonary interstitium and have diverse functions and characteristics in different lung conditions. In this review, we explore the heterogeneity of pulmonary fibroblasts during lung development, in healthy and pathological lungs. We also discuss their implications in fibrotic diseases, infectious diseases, and lung cancers, emphasizing the importance of comparative studies to understand their overlapping characteristics and signaling pathways.