Non-Canonical Wnt11 Signaling Regulates Pulmonary Fibrosis via Fibroblast and Alveolar Epithelial Type II Cell Crosstalk.

Francina Gonzalez De Los Santos, Akira Ando, Biao Hu, Alyssa Rosek, Sem H Phan, Tianju Liu

Abstract read

In one paragraph

Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed

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1 · What the graph read from it

What it found

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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.

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Francina Gonzalez De Los SantosGraduate Program in Immunology, University of Michigan, Ann Arbor, MI 48109, USA.

Akira AndoDepartment of Respiratory Medicine, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya 466-8550, Japan.ORCID 0000-0002-6762-039X

Biao HuDepartment of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.ORCID 0000-0002-4691-6490

Alyssa RosekDepartment of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.

Sem H PhanDepartment of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.

Tianju LiuDepartment of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.

Funding

National Institutes of Health- Heart, Lung and Blood Institute funded Dr. Sem Phan through the University of Michigan NIH grants HL14339 and HL138417

6 · The paper itself

Abstract

The reactivation of Wnt signaling pathways plays an important role in driving myofibroblast differentiation in fibrotic diseases; however, the mechanism is not clearly understood. In this study, we investigate the role of non-canonical Wnt11 signaling in human lung fibroblasts and its contributions to myofibroblast differentiation. Our results show that components of the non-canonical Wnt pathway are upregulated in bleomycin-induced pulmonary fibrosis and that in vivo depletion of Wnt11 in mouse lung fibroblasts significantly reduces lung fibrosis. Furthermore, co-culture studies using fibroblasts and alveolar type II epithelial cells (AECII) revealed a Wnt11-mediated mechanism that promotes myofibroblast differentiation. Finally, we demonstrate that in human lung fibroblasts, TGFβ can increases Wnt11 transcription by regulating Smad3 binding to the Wnt11 promoter and by modulating Wnt11 promoter activity. Together, these findings identify non-canonical Wnt11 as a regulator of myofibroblast differentiation and lung fibrosis.

Indexed as

Alveolar Epithelial CellsFibroblastsPulmonary FibrosisWnt ProteinsWnt Signaling PathwayAnimalsBleomycinCell DifferentiationCoculture TechniquesHumansLungMiceMyofibroblastsPromoter Regions, GeneticSmad3 ProteinBleomycinSmad3 ProteinWnt11 protein, humanWnt11 protein, mouseWnt Proteinsepithelial cell and fibroblast crosstalkfibrosisWnt11

Identifiers

PMID41516227

DOI10.3390/ijms27010351

PMCPMC12785642

What OpenQuestion holds

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LicenceCC BY

Read underepoch 390

Registered trials

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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.