ArticleiScience2026
RSK1-SRF signaling axis drives fibroblast activation and pulmonary fibrosis: Genetic causality and therapeutic targeting.
Article in iScience, 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary fibrosis is driven by persistent fibroblast activation and extracellular matrix (ECM) accumulation, yet upstream regulators that initiate and sustain these programs remain incompletely defined. Here, we tested whether the ribosomal S6 kinase 1-serum response factor (RSK1-SRF) axis contributes to idiopathic pulmonary fibrosis (IPF) and represents a tractable therapeutic target. Mendelian randomization supported a causal association between RSK1 and IPF risk, which aligned with increased RSK1 activity in human IPF lungs and bleomycin-injured mice. In lung fibroblasts, pharmacologic RSK1 inhibition blunted TGF-β-induced fibroblast-to-myofibroblast transition and ECM production. Mechanistically, RSK1 associated with SRF and promoted SRF phosphorylation and activation, thereby enhancing SRF-dependent profibrotic transcription.
Indexed as
Identifiers
What Socratic 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 Socratic graph.