ArticleJournal of the American Society of Nephrology : JASN2005
Role of matrix extracellular phosphoglycoprotein in the pathogenesis of X-linked hypophosphatemia.
Article in Journal of the American Society of Nephrology : JASN, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 90 citations in OpenAlex.
- A novel phex gene variant causes non-syndromic tooth agenesis.BMC oral health · 2025Article
- Bone marrow sinusoidal endothelial cells are a site of Fgf23 upregulation in a mouse model of iron deficiency anemia.Blood advances · 2023Article
- Article
- FGF23 is associated with early post-transplant hypophosphataemia and normalizes faster than iPTH in living donor renal transplant recipients: a longitudinal follow-up study.Clinical kidney journal · 2016Article
- Article
- An in situ hybridization study of perlecan, DMP1, and MEPE in developing condylar cartilage of the fetal mouse mandible and limb bud cartilage.European journal of histochemistry : EJH · 2015Article
- Article
- Hypophosphatemia and growth.Pediatric nephrology (Berlin, Germany) · 2013Review
- Mineralizing enthesopathy is a common feature of renal phosphate-wasting disorders attributed to FGF23 and is exacerbated by standard therapy in hyp mice.Endocrinology · 2012Article
- Overexpression of the DMP1 C-terminal fragment stimulates FGF23 and exacerbates the hypophosphatemic rickets phenotype in Hyp mice.Molecular endocrinology (Baltimore, Md.) · 2012Article
- Review
- Evidence for FGF23 involvement in a bone-kidney axis regulating bone mineralization and systemic phosphate and vitamin D homeostasis.Advances in experimental medicine and biology · 2012Review
- Regulation and function of the FGF23/klotho endocrine pathways.Physiological reviews · 2012Review
- Bone proteins PHEX and DMP1 regulate fibroblastic growth factor Fgf23 expression in osteocytes through a common pathway involving FGF receptor (FGFR) signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011Article
- Biomineralization of bone: a fresh view of the roles of non-collagenous proteins.Frontiers in bioscience (Landmark edition) · 2011Review
- ASARM peptides: PHEX-dependent and -independent regulation of serum phosphate.American journal of physiology. Renal physiology · 2011Article
- A Phe377del mutation in ANK leads to impaired osteoblastogenesis and osteoclastogenesis in a mouse model for craniometaphyseal dysplasia (CMD).Human molecular genetics · 2011Article
- Abnormal presence of the matrix extracellular phosphoglycoprotein-derived acidic serine- and aspartate-rich motif peptide in human hypophosphatemic dentin.The American journal of pathology · 2010Article
- ASARM mineralization hypothesis: a bridge too far?Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2010Article
- FGF-23 in bone biology.Pediatric nephrology (Berlin, Germany) · 2010Review
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
X-linked hypophosphatemia (XLH), a disorder characterized by hypophosphatemia, impaired skeletal mineralization, and aberrant regulation of 1, 25(OH)(2)D(3), is caused by inactivating mutations of Phex, which results in the accumulation of putative phosphaturic factors, called phosphatonins. Matrix extracellular phosphoglycoprotein (Mepe) is a proposed candidate for phosphatonin. The authors found that Hyp mice had increased expression of the MEPE and another phosphaturic factor, Fgf23. To establish MEPE's role in the pathogenesis of the XLH, Mepe-deficient mice were back-crossed onto the Hyp mouse homologue of XLH and phenotypes of wild-type, Mepe(-/-), Hyp, and Mepe(-/-)/Hyp mice were examined. Transfer of Mepe deficiency onto the Phex-deficient Hyp mouse background failed to correct hypophosphatemia and aberrant serum 1,25(OH)(2)D(3) levels. Increased Fgf23 levels in Hyp mice were not affected by superimposed Mepe deficiency. In addition, Mepe-deficient Hyp mice retained bone mineralization defects in vivo, characterized by decreased bone mineral density, reduced mineralized trabecular bone volume, lower flexural strength, and histologic evidence of osteomalacia; however, cultures of Hyp-derived bone marrow stromal cells in the absence of Mepe showed improved mineralization and normalization of osteoblast gene expression profiles observed in cells derived from Mepe-null mice. These results demonstrate that MEPE elevation in Hyp mice does not contribute to the hypophosphatemia associated with inactivating Phex mutations and is therefore not phosphatonin.
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