Article
Cell Biology
Shan Wang, Wei Rao, Ashley Hoffman, Jennifer Lin, Justin Li, Tao Lin, Audrey-Ann Liew, Matthew Vincent, Tinne C. J. Mertens, Harry Karmouty-Quintana, Christopher P. Crum, Mark L. Metersky, David A. Schwartz, Peter J. A. Davies, Clifford Stephan, Soma S. K. Jyothula, Ajay Sheshadri, Erik Eddie Suarez, Howard J. Huang, John F. Engelhardt, Burton F. Dickey, Kalpaj R. Parekh, Frank D. McKeon, Wa Xian
Summary: Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal lung disease characterized by fibrosis. The study found a specific stem cell variant in IPF that can transform normal lung fibroblasts into pathological myofibroblasts and activate and recruit myofibroblasts in xenograft models. This profibrotic stem cell variant expressed genes related to fibrosis and overlapped with abnormal epithelial signatures observed in previous single-cell RNA sequencing studies of IPF. The variant showed vulnerabilities to inhibitors of epidermal growth factor and mammalian target of rapamycin signaling, suggesting potential therapeutic targets.
SCIENCE TRANSLATIONAL MEDICINE
(2023)
Article
Respiratory System
Hak-Su Kim, Hyun Ju Yoo, Kwang Min Lee, Ha Eun Song, Su Jung Kim, Jae Ok Lee, Jung Jin Hwang, Jin Woo Song
Summary: This study identified lower levels of stearic acid in lung tissues of IPF patients and demonstrated its important role in inhibiting fibrotic marker expression and modulating profibrotic signaling. Stearic acid also exhibited antifibrotic effects in a mouse model of lung fibrosis.
Article
Respiratory System
Wanhai Qin, C. Arnold Spek, Brendon P. Scicluna, Tom van der Poll, JanWillem Duitman
Summary: This study found that deficiency of DNA methyltransferase DNMT3B promotes macrophage polarization during pulmonary fibrosis and enhances fibrosis development. The results suggest that myeloid DNMT3B plays a crucial role in inhibiting fibrotic macrophage polarization and protecting against bleomycin-induced pulmonary fibrosis.
RESPIRATORY RESEARCH
(2022)
Article
Biochemistry & Molecular Biology
Tatsuro Ogawa, Shigeyuki Shichino, Satoshi Ueha, Kana Bando, Kouji Matsushima
Summary: This study revealed the role of interstitial macrophages (IMs) in pulmonary fibrosis (PF) and their potential as a therapeutic target. IMs were found to have pro-fibrotic and anti-inflammatory properties in the fibrotic lungs. Depletion of C1q(+) IMs reduced activated fibroblasts and epithelial cells but worsened bodyweight loss and neutrophil infiltration in the silica-induced PF mouse model.
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
(2022)
Article
Respiratory System
Minxue Jia, Lorena Rosas, Maria G. Kapetanaki, Tracy Tabib, John Sebrat, Tamara Cruz, Anna Bondonese, Ana L. Mora, Robert Lafyatis, Mauricio Rojas, Panayiotis V. Benos
Summary: The study used single cell transcriptomics to investigate fibroblasts in patients with pulmonary fibrosis and healthy individuals. The findings revealed dysregulation of ribosomal proteins and copper-binding proteins in the early stage of pulmonary fibrosis. These new insights are crucial for understanding fibroblast plasticity, early diagnosis, and targeted therapeutic interventions.
RESPIRATORY RESEARCH
(2023)
Article
Respiratory System
Yoshinari Nakatsuka, Ai Yaku, Tomohiro Handa, Alexis Vandenbon, Yuki Hikichi, Yasutaka Motomura, Ayuko Sato, Masanori Yoshinaga, Kiminobu Tanizawa, Kizuku Watanabe, Toyohiro Hirai, Kazuo Chin, Yutaka Suzuki, Takuya Uehata, Takashi Mino, Tohru Tsujimura, Kazuyo Moro, Osamu Takeuchi
Summary: Regnase-1 is a critical post-transcriptional regulator of pulmonary immune homeostasis in mice, particularly in ILC2 cells. Deficiency of Regnase-1 leads to abnormal proliferation and activation of ILC2 cells, with upregulation of fibrosis-associated genes, ultimately enhancing bleomycin-induced pulmonary fibrosis.
EUROPEAN RESPIRATORY JOURNAL
(2021)
Article
Multidisciplinary Sciences
Abhalaxmi Singh, Sreeparna Chakraborty, Sing Wan Wong, Nicole A. Hefner, Andrew Stuart, Abdul S. Qadir, Amitabha Mukhopadhyay, Kurt Bachmaier, Jae-Won Shin, Jalees Rehman, Asrar B. Malik
Summary: This study explores the potential of mannose-targeted nanoparticles for treating lung fibrosis by delivering TGF beta-siRNA into profibrotic macrophages, inhibiting the development of fibrosis.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
(2022)
Article
Biochemistry & Molecular Biology
Jingyuan Liu, Zheng Pan, Boding Tong, Cong Wang, Jia Yang, Jingling Zou, Jikuan Jiang, Lusi Zhang, Bing Jiang
Summary: Artesunate, derived from Artemisia annua, was found to alleviate fibrosis and inhibit fibroblast activation through TGF-beta 1/SMAD2/3 and PI3K/Akt pathways in a rabbit glaucoma filtration surgery (GFS) model. It induced mitochondria-dependent ferroptosis in primary human ocular fibroblasts (OFs) by decreasing mitochondrial GPX4 expression and inhibiting other cellular ferroptosis defense mechanisms like FSP1 and Nrf2. This study suggests that artesunate may be a potential treatment for ocular fibrosis.
Article
Biochemistry & Molecular Biology
Michail Spathakis, Gesthimani Tarapatzi, Eirini Filidou, Leonidas Kandilogiannakis, Evangelos Karatzas, Paschalis Steiropoulos, Dimitrios Mikroulis, George M. Spyrou, Vangelis G. Manolopoulos, George Kolios, Konstantinos Arvanitidis
Summary: Niclosamide, a commonly used helminthicidic drug, has been shown to attenuate the abnormal expression of collagen and fibronectin induced by cytokine stimulation, suggesting its potential as a therapeutic agent against lung fibrosis.
Article
Physiology
Aritra Bhattacharyya, Kaveh Boostanpour, Mohamed Bouzidi, Liam Magee, Tian Y. Chen, Rachel Wolters, Paola Torre, Satish K. Pillai, Mallar Bhattacharya
Summary: This study reveals the involvement of CX3CR1+ monocyte-derived macrophages (moMacs) in bleomycin-induced lung fibrosis through the production of Pdgfa. Analysis at the single-cell level shows high expression of the receptor IL10-RA in moMacs from human fibrotic lungs. Furthermore, a novel IL10-dependent mechanism of macrophage polarization is identified.
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Yueming Cao, Jahnavi Rudrakshala, River Williams, Shade Rodriguez, Parand Sorkhdini, Alina X. Yang, Miles Mundy, Dongqin Yang, Amy Palmisciano, Thomas Walsh, Cesar Delcompare, Tanis Caine, Luca Tomasi, Barry S. Shea, Yang Zhou
Summary: This study investigated the role of the CHI3L1-CRTH2 pathway in the development of pulmonary fibrosis. The results showed that null mutation or inhibition of CRTH2 prevented the development of pulmonary fibrosis in mice. In addition, monocytes from patients with IPF appeared to be hyperresponsive to CHI3L1 stimulation. The findings support the targeting of the CHI3L1-CRTH2 pathway as a promising therapeutic approach for IPF and suggest that the sensitivity of blood monocytes to CHI3L1-induced profibrotic differentiation may serve as a biomarker for predicting treatment responsiveness.
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
(2022)
Article
Immunology
Ming-Li Zou, Ying-Ying Teng, Zhong-hua Chen, Si-Yu Liu, Yuan Jia, Kai-Wen Zhang, Jun-Jie Wu, Zheng-Dong Yuan, Xiao-Yu Tang, Shun Yu, Jun-Xing Ye, Xia Li, Xiao-Jin Zhou, Feng-Lai Yuan
Summary: Skin fibrosis is a common pathological feature of various diseases. The urokinase-type plasminogen activator (uPA) system, including uPA, urokinase plasminogen activator receptor (uPAR), and plasminogen activator inhibitor-1 (PAI-1), is upregulated in fibrotic diseases. The successful binding of uPA and uPAR activates the downstream peroxisome proliferator-activated receptor (PPAR) signaling pathway, reducing the proliferation, migration, and contraction of disease-derived fibroblasts and alleviating skin fibrosis. However, increased or robust upregulation of PAI-1 inhibits these effects, suggesting the involvement of PAI-1 in skin fibrosis.
FRONTIERS IN IMMUNOLOGY
(2022)
Review
Biochemistry & Molecular Biology
Mallar Bhattacharya
Summary: COVID-19 lung macrophages play a significant role in fibrotic remodeling, but more research is needed to fully understand their function.
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Huachun Cui, Na Xie, Sami Banerjee, Jing Ge, Dingyuan Jiang, Tapan Dey, Qiana L. Matthews, Rui-Ming Liu, Gang Liu
Summary: This study demonstrates that in lung fibrosis, myofibroblasts enhance glycolysis to produce lactate, which regulates the pathogenic phenotype of alveolar macrophages. Lactate induces profibrotic gene expression in macrophages, promoting the fibrotic process.
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
(2021)
Article
Cell Biology
Kaj E. C. Blokland, Habibie Habibie, Theo Borghuis, Greta J. Teitsma, Michael Schuliga, Barbro N. Melgert, Darryl A. Knight, Corry-Anke Brandsma, Simon D. Pouwels, Janette K. Burgess
Summary: Idiopathic pulmonary fibrosis (IPF) is a deadly lung disease with age being a major risk factor. Research suggests that ECM deposited by IPF fibroblasts does not induce cellular senescence, but rather leads to upregulation of proinflammatory and profibrotic cytokines, potentially contributing to the progression of fibrosis.
Article
Gastroenterology & Hepatology
Keely Marshall, Junfei Jin, Carl Atkinson, Ali Alawieh, Fei Qiao, Biao Lei, Kenneth D. Chavin, Songqing He, Stephen Tomlinson
Article
Cell Biology
Xin Wang, Justin Darcy, Chuan Cai, Junfei Jin, Andrzej Bartke, Deliang Cao
Article
Biochemistry & Molecular Biology
Yuekun Zhu, Chao Qu, Xuehui Hong, Yanyan Jia, Meihua Lin, Yunmei Luo, Fengqin Lin, Xiaolong Xie, Xiaoqi Xie, Juan Huang, Qin Wu, Xingfeng Qiu, Daxun Piao, Yanwei Xing, Tian Yu, Yuanfu Lu, Qiang Huang, Changyin Yu, Junfei Jin, Zhiyong Zhang
CELL DEATH AND DIFFERENTIATION
(2019)
Article
Pharmacology & Pharmacy
Qin-You Tan, Qian Hu, Sheng-Nan Zhu, Lu-Lu Jia, Juan Xiao, Hua-Zhen Su, Shao-Yuan Huang, Jing Zhang, Junfei Jin
Article
Cell Biology
Junfei Jin, Zhongyang Lu, Yanchun Li, Ji Hyun Ru, Maria F. Lopes-Virella, Yan Huang
JOURNAL OF LEUKOCYTE BIOLOGY
(2018)
Article
Biochemistry & Molecular Biology
Chenfei Huang, Zhe Cao, Jun Ma, Yi Shen, Yiwen Bu, Ramina Khoshaba, Guiyuan Shi, Dan Huang, Duan-Fang Liao, Haitao Ji, Junfei Jin, Deliang Cao
MOLECULAR CARCINOGENESIS
(2018)
Article
Multidisciplinary Sciences
Junfei Jin, Zhongyang Lu, Yanchun Li, L. Ashley Cowart, Maria F. Lopes-Virella, Yan Huang
Article
Medicine, Research & Experimental
Rong Wang, Wei Wang, Aili Li, Yongqin Wang, Junfei Jin, Zhaoquan Huang, Guojin Huang
EXPERIMENTAL AND THERAPEUTIC MEDICINE
(2019)
Article
Oncology
Huiping Qin, Guojin Huang, Feng Gao, Bin Huang, Die Wang, Xiaowen Hu, Yanni Wang, Ling Peng, Dan Luo, Biwen Mo, Chengping Hu, Yuanyuan Li, Changming Wang
EXPERIMENTAL CELL RESEARCH
(2019)
Article
Cell Biology
Wei Wang, Aili Li, Xiaodan Han, Qingqing Wang, Jinyong Guo, Youru Wu, Chen Wang, Guojin Huang
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
(2020)
Article
Oncology
Xiaodan Han, Aili Li, Wei Wang, Longxia Du, Chen Wang, Guojin Huang
Summary: MYG1 is upregulated in LUAD tissues and associated with poor prognosis, promoting proliferation, migration, and invasion of LUAD cells, while inhibiting autophagy through the AMP-activated protein kinase/mTOR complex 1 signaling pathway. MYG1 may serve as an oncogenic role in LUAD and be a potential therapeutic target for LUAD.
Article
Oncology
Chen Wang, Wei Wang, Xiaodan Han, Longxia Du, Aili Li, Guojin Huang
Summary: The study reveals that METTL1 is upregulated in LUAD tissues and associated with unfavorable prognosis, promoting proliferation and colony formation of A549 cells while inhibiting autophagy. It suggests that METTL1 acts as an oncogene in LUAD and may be a potential prognostic predictor and therapeutic target.
Article
Chemistry, Medicinal
Yi Gou, MeiRong Chen, Shanhe Li, JunGang Deng, Jinlong Li, GuiHua Fang, Feng Yang, GuoJin Huang
Summary: The three fluorescent dithiocarbazate-copper complexes showed significant cytotoxicity against pancreatic cancer cell lines, with complex 3 primarily targeting mitochondria and inducing cell death through mechanisms including ferroptosis. This complex is the first copper complex to demonstrate cellular events consistent with ferroptosis in cancer cells and effectively inhibited the growth of ASPC-1 cells in a mouse xenograft model.
JOURNAL OF MEDICINAL CHEMISTRY
(2021)
Article
Medicine, Research & Experimental
Longxia Du, Youru Wu, Xiaodan Han, Chen Wang, Aili Li, Guojin Huang
Summary: The NICE-3 protein has an oncogenic role in hepatocellular carcinoma, and in lung adenocarcinoma (LUAD) its high expression is associated with poor prognosis. Knockdown of NICE-3 in LUAD cells inhibits proliferation, migration, and invasion, while promoting autophagy. Additionally, NICE-3 knockdown suppresses AKT/mTORC1 signaling pathway in LUAD.
EXPERIMENTAL AND THERAPEUTIC MEDICINE
(2021)
Article
Chemistry, Physical
LiXia Hou, XiaoYing Jia, YouRu Wu, Jinlong Li, Dong Yao, Yi Gou, GuoJin Huang
Summary: Experimental results show that Cu(II) complexes 2 and 3 exhibit stronger anticancer activity than complex 1, with complex 3 being able to induce reactive oxygen species-mediated apoptotic cell death.
JOURNAL OF MOLECULAR STRUCTURE
(2021)