ReviewJournal of thoracic disease2026
Transcriptional factor KLF9 in pulmonary fibrosis: from molecular mechanisms to precision intervention-a narrative review.
Review in Journal of thoracic disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background and Objective: Pulmonary fibrosis (PF) is a devastating and progressive respiratory disease characterized by extracellular matrix (ECM) remodelling and functional decline, yet current therapeutic options remain limited. Recent studies have highlighted the critical, albeit complex, role of Krüppel-like factor 9 (KLF9) in the pathogenesis of PF. This review aims to comprehensively integrate the existing fragmented mechanistic evidence, delineate the differential regulatory networks of KLF9, and outline forward-looking strategies to promote the transition of KLF9 from a mechanistic candidate molecule to a clinically translatable target. Methods: A comprehensive literature search was conducted on databases including PubMed, Web of Science, and Embase for articles published up to March 14, 2026. The search focused on keywords such as ("pulmonary fibrosis" OR "idiopathic pulmonary fibrosis" OR "lung fibrosis") AND ("Krüppel-like factor 9" OR "KLF9" OR "BTEB1"). Key Content and Findings: Evidence indicates that KLF9 exhibits differential regulatory networks in alveolar epithelial cells, fibroblasts, and macrophages. Based on its functional paradox across diverse cell types, conventional systemic interventions targeting KLF9 face inherent limitations, including the "undruggable" nature of transcription factors and physical barriers in fibrotic lungs. To overcome these obstacles, advanced targeted strategies are required. Conclusions: While KLF9 plays a pivotal role in the fibrotic microenvironment, realizing its therapeutic potential necessitates a paradigm shift in intervention methods. Forward-looking strategies, including single-cell/spatial multi-omics analysis, ligand-modified inhaled nano-delivery, and stage-dependent dynamic dosing systems [such as proteolysis-targeting chimera (PROTAC) technology], represent promising avenues for precise KLF9 targeting in PF.
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.