ArticleRespiratory research2026
Protective effects of PRELP protein in a mouse model of pulmonary fibrosis.
Article in Respiratory research, 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
17 authors.
Funding
Abstract
backgroundPulmonary fibrosis is a chronic progressive lung disease characterized by extensive fibrosis and poor prognosis, highlighting the urgent need for novel therapeutic strategies. This study aims to elucidate the role of the small proteoglycan proline/arginine-rich end leucine-rich repeat protein (PRELP), evaluate the protective potential of recombinant PRELP protein, and investigate its underlying molecular mechanisms.
methodsRNA in situ hybridization was performed on lung sections prepared from control subjects and patients with idiopathic pulmonary fibrosis (IPF). In mouse experiments, we established a bleomycin (BLM)-induced lung fibrosis model using PRELP knockout mice and assessed the extent of fibrosis. Furthermore, we administered recombinant PRELP protein via the airway in wild-type mice with BLM-induced fibrosis to evaluate its effects. In vitro experiments were conducted to investigate the role of PRELP in alveolar epithelial cells and fibroblasts.
resultsIn human lungs, PRELP expression was mainly detected in stromal regions and partly in type 2 alveolar epithelial cells. Furthermore, PRELP was broadly expressed in alveolar areas of controls but was markedly reduced in the alveolar region and localized to vessel walls in IPF patients. In mouse experiments, fibrosis was more severe in PRELP knockout mice after BLM intratracheal administration than in wild-type mice. Notably, prophylactic trans-airway administration of recombinant PRELP suppressed BLM-induced fibrosis in wild-type mice in vivo. In vitro experiments revealed that PRELP suppresses the acquisition of mesenchymal traits and enhances the maintenance of epithelial cell function in epithelial cells, while inhibiting the migratory ability of fibroblast cells. Mechanistically, PRELP suppressed fibrotic changes in epithelial cells not only through the transforming growth factor-beta (TGF-β) pathway but also via Receptor for advanced glycation end products (RAGE)/ Diaphanous 1 (DIAPH1)/ Yes-associated protein (YAP) signaling axis.
conclusionsThe small proteoglycan PRELP plays a pivotal role in a mouse model of pulmonary fibrosis by suppressing the upregulation of mesenchymal markers, reinforcing epithelial cell function, and inhibiting fibroblast migration. Notably, prophylactic trans-airway administration of recombinant PRELP protected against pulmonary fibrosis, indicating that PRELP may be a promising novel protective agent for this disease.
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.