ReviewMolecular aspects of medicine2019
Developmental pathways in the pathogenesis of lung fibrosis.
Review in Molecular aspects of medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 268 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
268 citing papers in PubMed, 1 synthesis or guideline pooled it, 512 citations in OpenAlex.
- Genetic characterization of preschool wheeze phenotypes.The Journal of allergy and clinical immunology · 2025Pooled it
- A small-molecule TNIK inhibitor targets fibrosis in preclinical and clinical models.Nature biotechnology · 2025Trial
- A Clinical Multicenter Trial of Recombinant Human Interferon Gamma in Tuberculosis (GAM2022): Experience with the Use of Human Recombinant Interferon Gamma in TB Practice.Infectious disorders drug targets · 2025Trial
- Injectable microsphere-based delivery strategies for stem cells and their derivatives in tissue regeneration.Bioactive materials · 2026Review
- Bicyclol: A Useful Agent for Silicosis?International journal of molecular sciences · 2026Review
- mExperimental and therapeutic medicine · 2026Review
- A FGFR3 decoy receptor attenuates lung fibroblast-to-myofibroblast transition and pulmonary fibrosis.American journal of respiratory cell and molecular biology · 2026Article
- β-carboline derivative Z86 alleviates pulmonary fibrosis via suppressing TGF-β/Smad signaling.Natural products and bioprospecting · 2026Article
- Extracellular vesicles in senescence-associated chronic lung diseases.Chinese medical journal · 2026Review
- Sustained YAP/TAZ activation promotes aberrant alveolar epithelial cell differentiation and drives persistent fibrotic remodeling.JCI insight · 2026Article
- Norcantharidin attenuates amiodarone-induced pulmonary fibrosis via modulating miRNA-30a/GSK-3β/β-catenin and oxidative-inflammatory pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Article
- Recent advances in pulmonary fibrosis: from lung surfactant to the immune connection.Respiratory research · 2026Review
- LncRNA HOXA11-AS promotes idiopathic pulmonary fibrosis progression via sponging miR-148a-3p and regulating SMAD2.Hereditas · 2026Article
- Testosterone protects from metabolic syndrome-associated lung dysfunction in a high-fat diet rabbit model.Endocrinology · 2026Article
- Circular RNA circSmad4 controls pulmonary fibrosis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026Article
- The CaInternational journal of molecular sciences · 2026Article
- Effects of the WNT signaling pathway on inflammation and fibrosis in idiopathic pulmonary fibrosis: Clinical, radiological and molecular evaluation.Experimental and therapeutic medicine · 2026Article
- Crizotinib attenuates bleomycin-induced pulmonary fibrosis via regulating fibroblast activation.Journal of thoracic disease · 2026Article
- Modulation of endothelial-to-mesenchymal transition via NRP-1 targeting with melittin attenuates pulmonary fibrosis.Materials today. Bio · 2026Article
208 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive and terminal lung disease with no known cure. IPF is a disease of aging, with median age of diagnosis over 65 years. Median survival is between 3 and 5 years after diagnosis. IPF is characterized primarily by excessive deposition of extracellular matrix (ECM) proteins by activated lung fibroblasts and myofibroblasts, resulting in reduced gas exchange and impaired pulmonary function. Growing evidence supports the concept of a pro-fibrotic environment orchestrated by underlying factors such as genetic predisposition, chronic injury and aging, oxidative stress, and impaired regenerative responses may account for disease development and persistence. Currently, two FDA approved drugs have limited efficacy in the treatment of IPF. Many of the genes and gene networks associated with lung development are induced or activated in IPF. In this review, we analyze current knowledge in the field, gained from both basic and clinical research, to provide new insights into the disease process, and potential approaches to treatment of pulmonary fibrosis.
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What OpenQuestion holds
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.