ReviewExpert opinion on therapeutic targets2019
New therapeutics based on emerging concepts in pulmonary fibrosis.
Review in Expert opinion on therapeutic targets, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- The Role of the Multidisciplinary Evaluation of Interstitial Lung Diseases: Systematic Literature Review of the Current Evidence and Future Perspectives.Frontiers in medicine · 2019Pooled it
- Transcriptional factor KLF9 in pulmonary fibrosis: from molecular mechanisms to precision intervention-a narrative review.Journal of thoracic disease · 2026Review
- A Multispecies, Modality-Agnostic Scalable In Vivo Mosaic Screening Platform for Therapeutic Target Discovery.bioRxiv : the preprint server for biology · 2026Article
- PLK1 inhibition by volasertib suppresses key transcriptional regulators underlying fibroblast activation and pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Wilms tumor 1 impairs apoptotic clearance of fibroblasts in distal fibrotic lung lesions.The Journal of clinical investigation · 2025Article
- SEMA3B inhibits TGFβ-induced extracellular matrix protein production and its reduced levels are associated with a decline in lung function in IPF.American journal of physiology. Cell physiology · 2024Article
- Geniposide ameliorates bleomycin-induced pulmonary fibrosis in mice by inhibiting TGF-β/Smad and p38MAPK signaling pathways.PloS one · 2024Article
- Up-regulation by overexpression of c-MET in fibroblastic foci of usual interstitial pneumonia.Pathologica · 2023Article
- Design of a phase III, double-blind, randomised, placebo-controlled trial of BI 1015550 in patients with idiopathic pulmonary fibrosis (FIBRONEER-IPF).BMJ open respiratory research · 2023Article
- Pulmonary Fibrosis: Unveiling the Pathogenesis, Exploring Therapeutic Targets, and Advancements in Drug Delivery Strategies.AAPS PharmSciTech · 2023Review
- Wilms Tumor 1-Driven Fibroblast Activation and Subpleural Thickening in Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2023Review
- The Role of Nrf2 in Pulmonary Fibrosis: Molecular Mechanisms and Treatment Approaches.Antioxidants (Basel, Switzerland) · 2022Review
- ASK1ng to Delay the Progression of Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2022Article
- Natural Product-Based Potential Therapeutic Interventions of Pulmonary Fibrosis.Molecules (Basel, Switzerland) · 2022Review
- Dysregulated overexpression of Sox9 induces fibroblast activation in pulmonary fibrosis.JCI insight · 2021Article
- Review
- Article
- Notch3: A New Culprit in Fibrotic Lung Disease.American journal of respiratory cell and molecular biology · 2021Article
- Review
- Silencing Heat Shock Protein 47 (HSP47) in Fibrogenic Precision-Cut Lung Slices: A Surprising Lack of Effects on Fibrogenesis?Frontiers in medicine · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
introductionFibrosis is an irreversible pathological endpoint in many chronic diseases, including pulmonary fibrosis. Idiopathic pulmonary fibrosis (IPF) is a progressive and often fatal condition characterized by (myo)fibroblast proliferation and transformation in the lung, expansion of the extracellular matrix, and extensive remodeling of the lung parenchyma. Recent evidence indicates that IPF prevalence and mortality rates are growing in the United States and elsewhere. Despite decades of research on the pathogenic mechanisms of pulmonary fibrosis, few therapeutics have succeeded in the clinic, and they have failed to improve IPF patient survival. Areas covered: Based on a literature search and our own results, we discuss the key cellular and molecular responses that contribute to (myo)fibroblast actions and pulmonary fibrosis pathogenesis; this includes signaling pathways in various cells that aberrantly and persistently activate (myo)fibroblasts in fibrotic lesions and promote scar tissue formation in the lung. Expert opinion: Lessons learned from recent failures and successes with new therapeutics point toward approaches that can target multiple pro-fibrotic processes in IPF. Advances in preclinical modeling and single-cell genomics will also accelerate novel discoveries for effective treatment of IPF.
Indexed as
Identifiers
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.