Review
Biology
Mahmoud Aghaei, Sanaz Dastghaib, Sajjad Aftabi, Mohamad-Reza Aghanoori, Javad Alizadeh, Pooneh Mokarram, Parvaneh Mehrbod, Milad Ashrafizadeh, Ali Zarrabi, Kielan Darcy McAlinden, Mathew Suji Eapen, Sukhwinder Singh Sohal, Pawan Sharma, Amir A. Zeki, Saeid Ghavami
Summary: The disruption of protein homeostasis in lung cells by stressors leads to activation of the unfolded protein response (UPR) to manage the increased functional demands. Dysregulation of UPR and ER stress are implicated in various human diseases. Compounds targeting the UPR pathway are being considered as potential therapies.
Article
Critical Care Medicine
Anna Duckworth, Michael A. Gibbons, Richard J. Allen, Howard Almond, Robin N. Beaumont, Andrew R. Wood, Katie Lunnon, Mark A. Lindsay, Louise Wain, Jess Tyrrell, Chris J. Scotton
Summary: Using mendelian randomisation, this study found that shorter telomere length is associated with higher odds of IPF but not COPD, suggesting a potential contributory factor in IPF and differing mechanisms in COPD.
LANCET RESPIRATORY MEDICINE
(2021)
Article
Oncology
Shashipavan Chillappagari, Julian Schwarz, Vidyasagar Kesireddy, Jessica Knoell, Martina Korfei, Konrad Hoetzenecker, M. Lienhard Schmitz, Christian Behl, Saverio Bellusci, Andreas Guenther, Poornima Mahavadi
Summary: This study found that modulation of autophagy regulating proteins can be used as a therapeutic strategy for idiopathic pulmonary fibrosis (IPF). By improving autophagy and reducing fibroblast proliferation, fine tuning of this pathway may improve antifibrotic properties and enhance the efficacy of current IPF therapy.
CLINICAL AND TRANSLATIONAL MEDICINE
(2022)
Article
Cardiac & Cardiovascular Systems
Kevin Bray, Sandeep Bodduluri, Young-il Kim, Vivek Sthanam, Hrudaya Nath, Surya P. Bhatt
Summary: Previous studies have shown that low forced expiratory volume in one second (FEV1) is associated with coronary artery disease (CAD). This study aimed to investigate if low FEV1 due to airflow obstruction or ventilatory restriction have different associations with CAD.
RESPIRATORY MEDICINE
(2023)
Article
Medicine, General & Internal
Qiang Zhang, Yuanyi Yue, Rui Zheng
Summary: In this study, differentially expressed proteins (DEPs) were identified between COPD patients and normal smokers using iTRAQ-based proteomic analysis. Clusterin (CLU) was identified as a potential serum biomarker candidate. CLU levels were significantly increased in COPD patients and correlated with lung function and imaging parameters. Additionally, cigarette smoke extract (CSE) treatment promoted lung fibroblast activation and fibrosis, which was partially reversed by CLU silencing.
CHINESE MEDICAL JOURNAL
(2022)
Article
Medicine, Research & Experimental
Jade Jaffar, Ian Glaspole, Karen Symons, Glen Westall
Summary: Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with poor prognosis, and the transcription factor NF-ΚB is suggested as a potential therapeutic target. ACT001, an NF-ΚB inhibitor, showed inhibitory effects on fibroblast activity in primary lung fibroblasts from patients with and without IPF, indicating its potential as a therapeutic agent for IPF.
BIOMEDICINE & PHARMACOTHERAPY
(2021)
Article
Biochemistry & Molecular Biology
Ulf Hedstrom, Lisa Oberg, Outi Vaarala, Goran Dellgren, Martin Silverborn, Leif Bjermer, Gunilla Westergren-Thorsson, Oskar Hallgren, Xiaohong Zhou
Summary: The study found that airway epithelial cells in patients with Chronic Obstructive Pulmonary Disease (COPD) are damaged, and COPD epithelial cells show differential gene expression on COPD airway scaffolds compared to normal epithelial cells, with increased proliferation and maintained basal cell phenotype.
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
(2021)
Review
Cell Biology
Shengnan Yang, Peipei Liu, Yale Jiang, Zai Wang, Huaping Dai, Chen Wang
Summary: Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with unknown causes, and currently the only medications that can slow down the progression of the disease and improve survival rate are pirfenidone and nintedanib. The use of mesenchymal stem cells (MSCs) provides a new hope for treating interstitial lung disease, but optimal treatment protocols are still lacking.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Article
Cell Biology
Ashesh Chakraborty, Michal Mastalerz, Meshal Ansari, Herbert B. Schiller, Claudia A. Staab-Weijnitz
Summary: This review investigates the alterations in airway epithelial cells in idiopathic pulmonary fibrosis (IPF) and highlights their significant role in disease development. The findings support further exploration of therapeutic strategies targeting these alterations, which represent important future research directions.
Review
Pharmacology & Pharmacy
Qianru Mei, Zhe Liu, He Zuo, Zhenhua Yang, Jing Qu
Summary: Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal lung disease with limited understanding of its pathogenesis. Recent studies suggest that sustained lung epithelial injury and fibroblast differentiation play key roles in the development of IPF. Current treatments can slow disease progression but cannot cure it.
FRONTIERS IN PHARMACOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Yue Zhang, Wenhui Huang, Zemao Zheng, Wei Wang, Yafei Yuan, Qiaohui Hong, Jiajia Lin, Xu Li, Ying Meng
Summary: Cigarette smoke induces senescence of AT2 cells via a SIRT1/autophagy dependent pathway, involving mitochondrial reactive oxygen species and DNA damage. Activating SIRT1 can reduce senescence by promoting autophagy.
FREE RADICAL BIOLOGY AND MEDICINE
(2021)
Review
Biochemistry & Molecular Biology
Yue Yu, Ailin Yang, Ganggang Yu, Haoyan Wang
Summary: This review explores the relationship between ER stress and UPR with COPD, as well as drug intervention strategies targeting the UPR pathway in COPD. By analyzing other cellular processes, new therapeutic approaches and preventive measures for COPD are investigated.
Review
Biochemistry & Molecular Biology
Shanshan Liu, Chang Liu, Qianrong Wang, Suosi Liu, Jiali Min
Summary: Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive respiratory disease characterized by irreversible decline in lung function. The dysregulated expression of chemokines and chemokine receptors has been associated with the development and progression of IPF. Chemokines of the CC family play significant roles in exacerbating IPF progression. Modulating levels of detrimental CC chemokines and interrupting the corresponding transduction axis by neutralizing antibodies or antagonists are potential treatment options for IPF. This review focuses on the roles of different CC chemokines in IPF pathogenesis and their potential use as biomarkers or therapeutic targets.
Article
Immunology
Lijing Wang, Qiong Chen, Qiao Yu, Jian Xiao, Hongjun Zhao
Summary: In this study, it was found that exosomes derived from cigarette smoke extract-treated mouse airway epithelial cells promoted M1 macrophage polarization by upregulating TREM-1 expression, thereby aggravating the development of COPD.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2021)
Article
Medicine, General & Internal
Marissa Wisman, Mehmet Nizamoglu, Jacobien A. Noordhoek, Wim Timens, Janette K. Burgess, Irene H. Heijink
Summary: In idiopathic pulmonary fibrosis (IPF), disturbed crosstalk between alveolar progenitor cells and the stromal niche impairs regenerative capacity, potentially contributing to alveolar impairment. Organoid cultures from IPF lungs showed lower numbers and larger size compared to non-IPF lungs, indicating impaired crosstalk between supportive cells and epithelial cells. These findings suggest that disturbed interactions within the stromal micro-environment lead to abnormal alveolar repair and fibrosis in IPF.
FRONTIERS IN MEDICINE
(2023)
