ArticleAnnals of medicine2026
FGF8 alleviates LPS-induced acute lung injury
Article in Annals of medicine, 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
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute lung injury (ALI) and progressive acute respiratory distress syndrome (ARDS) have high mortality and limited effective therapies. Fibroblast growth factor 8 (FGF8) participates in lung development, inflammation and cell regulation, yet its function in ALI remains unclear.
methodsWe constructed an LPS-induced mouse ALI model to detect FGF8 expression. FGF8 haploinsufficiency and overexpression systems were used to explore its biological function. RNA-seq combined with GO and KEGG enrichment analyses screened target pathways, which were further verified via experiments. The PPARγ antagonist GW9662 was applied to confirm the regulatory role of PPARγ.
resultsLung FGF8 expression was significantly upregulated in LPS-challenged mice. FGF8 haploinsufficiency exacerbated weight loss, pulmonary edema, lung histological injury, pro-inflammatory cytokine (IL-1β, IL-6, TNF-α) release, and apoptosis imbalance. It also accelerated collagen accumulation and elevated profibrotic markers including α-SMA, TGF-β1 and COL1A1. Conversely, FGF8 overexpression relieved all these pathological phenotypes. Mechanistically, FGF8 haploinsufficiency inhibited PPARγ and activated ERK1/2 phosphorylation, while FGF8 overexpression reversed this change. Blocking PPARγ with GW9662 further boosted ERK1/2 activation and abolished the protective effects of FGF8 against ALI.
conclusionFGF8 alleviates inflammation, apoptosis and early pulmonary fibrosis in LPS-induced ALI mice via the PPARγ/ERK1/2 signaling pathway.
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.