ArticleScience translational medicine2015
Modeling pulmonary alveolar microlithiasis by epithelial deletion of the Npt2b sodium phosphate cotransporter reveals putative biomarkers and strategies for treatment.
Article in Science translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 2 of them syntheses that pooled it.
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Who cites it
33 citing papers in PubMed, 2 syntheses or guidelines pooled it, 60 citations in OpenAlex.
- New insights in the genetic variant spectrum of SLC34A2 in pulmonary alveolar microlithiasis; a systematic review.Orphanet journal of rare diseases · 2023Pooled it
- Differences in genetic characteristics between Chinese and non-Chinese patients with pulmonary alveolar microlithiasis-case series and a systematic review.Therapeutic advances in respiratory diseasePooled it
- Cell Calcification Models and Their Implications for Medicine and Biomaterial Research.Advanced healthcare materials · 2026Review
- Donor-dependent heterogeneity and matrix-remodeling transcriptional programs inFrontiers in cell and developmental biology · 2026Article
- Hydroxyapatite microspheres induce durable pleurodesis and are rapidly cleared by pleural osteoclasts.JCI insight · 2025Article
- Soft tissue calcifications in chronic kidney disease-beyond the vasculature.Pflugers Archiv : European journal of physiology · 2025Review
- Pulmonary osteoclast-like cells in silica induced pulmonary fibrosis.Science advances · 2024Article
- Phosphate in Cardiovascular Disease: From New Insights Into Molecular Mechanisms to Clinical Implications.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Pharmacology of Mammalian NaHandbook of experimental pharmacology · 2024Article
- Effects of the novel sodium-dependent phosphate cotransporter 2b inhibitor DZ1462 on hyperphosphatemia in chronic kidney disease.American journal of translational research · 2024Article
- TRIB3 promotes pulmonary fibrosis through inhibiting SLUG degradation by physically interacting with MDM2.Acta pharmaceutica Sinica. B · 2023Article
- Insights into pulmonary phosphate homeostasis and osteoclastogenesis emerge from the study of pulmonary alveolar microlithiasis.Nature communications · 2023Article
- Pulmonary osteoclast-like cells in silica induced pulmonary fibrosis.bioRxiv : the preprint server for biology · 2023Article
- A dissemination-prone morphotype enhances extrapulmonary organ entry by Cryptococcus neoformans.Cell host & microbe · 2022Article
- Impaired phosphate transport in SLC34A2 variants in patients with pulmonary alveolar microlithiasis.Human genomics · 2022Article
- Pulmonary Alveolar Microlithiasis - A Review.The Yale journal of biology and medicine · 2021Review
- Extracellular phosphate enhances the function of F508del-CFTR rescued by CFTR correctors.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2021Article
- Treatment of air leakage using the VIO soft coagulation system: a mouse pulmonary air leak model.Surgery today · 2021Article
- Constitutive depletion of Slc34a2/NaPi-IIb in rats causes perinatal mortality.Scientific reports · 2021Article
- Pulmonary alveolar microlithiasis.European respiratory review : an official journal of the European Respiratory Society · 2020Review
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Authors and funding
17 authors at 2 institutions in 1 country.
Funding
Abstract
Pulmonary alveolar microlithiasis (PAM) is a rare, autosomal recessive lung disorder associated with progressive accumulation of calcium phosphate microliths. Inactivating mutations in SLC34A2, which encodes the NPT2b sodium-dependent phosphate cotransporter, has been proposed as a cause of PAM. We show that epithelial deletion of Npt2b in mice results in a progressive pulmonary process characterized by diffuse alveolar microlith accumulation, radiographic opacification, restrictive physiology, inflammation, fibrosis, and an unexpected alveolar phospholipidosis. Cytokine and surfactant protein elevations in the alveolar lavage and serum of PAM mice and confirmed in serum from PAM patients identify serum MCP-1 (monocyte chemotactic protein 1) and SP-D (surfactant protein D) as potential biomarkers. Microliths introduced by adoptive transfer into the lungs of wild-type mice produce marked macrophage-rich inflammation and elevation of serum MCP-1 that peaks at 1 week and resolves at 1 month, concomitant with clearance of stones. Microliths isolated by bronchoalveolar lavage readily dissolve in EDTA, and therapeutic whole-lung EDTA lavage reduces the burden of stones in the lungs. A low-phosphate diet prevents microlith formation in young animals and reduces lung injury on the basis of reduction in serum SP-D. The burden of pulmonary calcium deposits in established PAM is also diminished within 4 weeks by a low-phosphate diet challenge. These data support a causative role for Npt2b in the pathogenesis of PAM and the use of the PAM mouse model as a preclinical platform for the development of biomarkers and therapeutic strategies.
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