ReviewLife (Basel, Switzerland)2020
The ER Stress/UPR Axis in Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis.
Review in Life (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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Who cites it
39 citing papers in PubMed, 59 citations in OpenAlex.
- Pan-cancer analysis reveals differential PERK expression across tumour types and its potential as a therapeutic target.Discover oncology · 2026Article
- Selective activation of the unfolded protein response and proteolytic pathways in sarcopenic limb muscles of bronchiectasis patients.ERJ open research · 2026Article
- A systematic review on the potential of modulating the IRE arm of the UPR in U87 and U251 glioblastoma cells for improved therapeutic efficacy.Molecular biology research communications · 2026Review
- Endoplasmic Reticulum Stress as a Stage-Dependent Regulatory Hub in Rheumatoid Arthritis.Journal of inflammation research · 2026Review
- The intersection of liver cirrhosis and pulmonary fibrosis.Journal of translational medicine · 2025Review
- TRIB3 Links Endoplasmic Reticulum Stress to Impaired Efferocytosis in Atherosclerosis.Circulation research · 2025Article
- The Role of Endoplasmic Reticulum Stress in the Development of Periodontitis-From Experimental Cell and Animal Models to Humans.International journal of molecular sciences · 2025Review
- Reciprocal Regulation Between the SCFbioRxiv : the preprint server for biology · 2025Article
- Effect of 30-day Ramadan fasting on autophagy pathway and metabolic health outcome in healthy individuals.Molecular biology research communications · 2025Article
- Organellar quality control crosstalk in aging-related disease: Innovation to pave the way.Aging cell · 2025Review
- Identification of key genes associated with idiopathic pulmonary fibrosis and sarcopenia by bioinformatics analysis.PloS one · 2025Article
- Targeting the self-amplifying loop between ATF6 and SNAI1 to inhibit epithelial‒mesenchymal transition in fibrotic lesions.Theranostics · 2025Article
- ER stress genes (Frontiers in immunology · 2025Article
- Current advancements in the mechanisms and animal models of acute exacerbation of pulmonary fibrosis: a systematic review.Frontiers in pharmacology · 2025Review
- Endoplasmic reticulum stress in non-small cell lung cancer.American journal of cancer research · 2025Review
- Mitochondria associated membranes in dilated cardiomyopathy: connecting pathogenesis and cellular dysfunction.Frontiers in cardiovascular medicine · 2025Review
- The protein disulfide isomerase A3 and osteopontin axis promotes influenza-induced lung remodelling.British journal of pharmacology · 2024Article
- RHBDF1 promotes PERK expression through the JNK/FoxO3 pathway in breast cancer cells.Acta biochimica et biophysica Sinica · 2024Article
- The modulation of autophagy and unfolded protein response by ent-kaurenoid derivative CPUK02 in human colorectal cancer cells.Molecular biology reports · 2024Article
- Platelet Activating Factor Receptor and Intercellular Adhesion Molecule-1 Expression Increases in the Small Airway Epithelium and Parenchyma of Patients with Idiopathic Pulmonary Fibrosis: Implications for Microbial Pathogenesis.Journal of clinical medicine · 2024Article
Corrections and comments
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Authors and funding
15 authors at 9 institutions in 5 countries.
Funding
Abstract
Cellular protein homeostasis in the lungs is constantly disrupted by recurrent exposure to various external and internal stressors, which may cause considerable protein secretion pressure on the endoplasmic reticulum (ER), resulting in the survival and differentiation of these cell types to meet the increased functional demands. Cells are able to induce a highly conserved adaptive mechanism, known as the unfolded protein response (UPR), to manage such stresses. UPR dysregulation and ER stress are involved in numerous human illnesses, such as metabolic syndrome, fibrotic diseases, and neurodegeneration, and cancer. Therefore, effective and specific compounds targeting the UPR pathway are being considered as potential therapies. This review focuses on the impact of both external and internal stressors on the ER in idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD) and discusses the role of the UPR signaling pathway activation in the control of cellular damage and specifically highlights the potential involvement of non-coding RNAs in COPD. Summaries of pathogenic mechanisms associated with the ER stress/UPR axis contributing to IPF and COPD, and promising pharmacological intervention strategies, are also presented.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.