ArticleRMD open2026
Anlotinib ameliorates myositis-associated interstitial lung disease (MAILD) via suppression of the NETs-PI3K/Akt-driven epithelial-mesenchymal transition.
Article in RMD open, 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
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMyositis-associated interstitial lung disease (MAILD) is one of the most severe complications of idiopathic inflammatory myopathy, characterised by rapidly progressive pulmonary fibrosis and high mortality. Treatment options are limited, and mechanisms driving epithelial-mesenchymal transition (EMT) in MAILD are incompletely understood. Anlotinib, a multitarget tyrosine kinase inhibitor, shows potential in fibrotic diseases; however, its role and mechanism in MAILD need clarification.
methodsTo assess anlotinib's therapeutic effects, we established a MAILD mouse model and a neutrophil extracellular trap (NET)-induced human alveolar epithelial cell (A549) model. H&E and Masson staining analysed lung pathological changes and collagen deposition. Immunohistochemistry, immunofluorescence and Western blot detected expressions of NETs markers (myeloperoxidase, citrullinated histone H3), phosphatidylinositol 3-kinase/protein kinase B (PI3K)/Akt components and EMT markers (E-cadherin, α-smooth muscle actin). RNA sequencing and gene set enrichment analysis identified differentially expressed genes and signalling pathways. Cell counting kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU) and wound healing assays assessed cellular repair and migration.
resultsMAILD mouse lungs showed structural damage, inflammatory infiltration, collagen deposition, increased NETs formation, PI3K/Akt activation and enhanced EMT. Anlotinib significantly ameliorated pulmonary fibrosis and reduced pro-inflammatory cytokines (tumour necrosis factor-α (TNF-α), interleukin (IL)-6, IL-1β). In vivo and in vitro, anlotinib suppressed NETs formation, PI3K/Akt activation and EMT, while enhancing alveolar epithelial cell repair and migration.
conclusionAnlotinib alleviates MAILD progression by inhibiting the NETs-PI3K/Akt axis and subsequent EMT, providing a theoretical basis for drug repurposing and supporting its clinical translation potential in MAILD.
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.