ArticleNature communications2022
Tartrate-resistant acid phosphatase 5 promotes pulmonary fibrosis by modulating β-catenin signaling.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed.
- Integrin αVβ3 as a context‑dependent regulator of bone homeostasis: Insights into osteoporosis pathogenesis and therapeutic targeting (Review).Molecular medicine reports · 2026Review
- MXene-integrated quantum dots: an innovative tool for next-generation healthcare applications.Nanoscale advances · 2026Review
- ACP5-positive macrophages contribute to cerebral oedema and neuroinflammation after traumatic brain injury.Clinical and translational medicine · 2026Article
- Exploring the Molecular Mechanisms of SB216763 in the Therapeutic Intervention of Pulmonary Fibrosis Based on Macrophage Functional Plasticity.Fundamental & clinical pharmacology · 2026Article
- Plasma apolipoprotein E protein attenuates pulmonary fibrosis through LRP1 and PLAU dual receptor-mediated TGF-β/Smad inhibition.Journal of advanced research · 2026Article
- Therapeutic modulation of the vitreoretinal fibrosis microenvironment in female mice using engineered macrophage-derived extracellular vesicles.Nature communications · 2026Article
- Cerebrovascular vulnerability and fibrosis in human brain aneurysms.Nature neuroscience · 2026Article
- Evidence for PDZ-Binding Kinase in Lung Disease With an Emphasis on PAH.Pulmonary circulation · 2026Review
- Article
- Danthron prevents pulmonary fibrosis through improving mitochondrial function by upregulating carboxylesterase 3.Respiratory research · 2026Article
- Legumain Restrains Granuloma Formation by Inhibiting mTORC1/STAT1-Mediated M1 Macrophage Polarization in Sarcoidosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Single-cell profiling and machine learning identify cuproptosis-related fibroblast subpopulations and fibrogenesis modulator AEBP1 in endometriosis.Apoptosis : an international journal on programmed cell death · 2026Article
- TRAP5 Inhibition Targeting Scar-Associated Macrophages Ameliorates Acute Kidney Injury to Chronic Kidney Disease Transition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Pharmacological mechanism of active components inFrontiers in pharmacology · 2026Article
- Polystyrene-associated pulmonary fibrosis: a summary based on the available evidence and prospects.Frontiers in immunology · 2026Review
- Nanocarrier-Enabled siRNA Therapy for Pulmonary Fibrosis: Pharmacological Rationale, Delivery Barriers, and Translational Opportunities.International journal of nanomedicine · 2026Review
- Overexpression of the lncRNA TUG1 regulates high-glucose-induced endocytic clearance dysfunction in HLSECs via the Wnt/β-catenin signaling pathway.European journal of medical research · 2025Article
- CILP attenuates pulmonary fibrosis through the TGF-β1/SMAD3 pathway.European journal of medical research · 2025Article
- Review
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF) is a fatal interstitial lung disease with limited therapeutic options. Tartrate-resistant acid phosphatase 5 (ACP5) performs a variety of functions. However, its role in IPF remains unclear. Here, we demonstrate that the levels of ACP5 are increased in IPF patient samples and mice with bleomycin (BLM)-induced pulmonary fibrosis. In particular, higher levels of ACP5 are present in the sera of IPF patients with a diffusing capacity of the lungs for carbonmonoxide (DLCO) less than 40% of the predicted value. Additionally, Acp5 deficiency protects mice from BLM-induced lung injury and fibrosis coupled with a significant reduction of fibroblast differentiation and proliferation. Mechanistic studies reveal that Acp5 is upregulated by transforming growth factor-β1 (TGF-β1) in a TGF-β receptor 1 (TGFβR1)/Smad family member 3 (Smad3)-dependent manner, after which Acp5 dephosphorylates p-β-catenin at serine 33 and threonine 41, inhibiting the degradation of β-catenin and subsequently enhancing β-catenin signaling in the nucleus, which promotes the differentiation, proliferation and migration of fibroblast. More importantly, the treatment of mice with Acp5 siRNA-loaded liposomes or Acp5 inhibitor reverses established lung fibrosis. In conclusions, Acp5 is involved in the initiation and progression of pulmonary fibrosis and strategies aimed at silencing or suppressing Acp5 could be considered as potential therapeutic approaches against pulmonary fibrosis.
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