Evidence map›Paper›PMID 19520780›Full record

ArticleEndocrinology2009

Matrix extracellular phosphoglycoprotein (MEPE) is a new bone renal hormone and vascularization modulator.

Valentin David, Aline Martin, Anne-Marie Hedge, Peter S N Rowe

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
4.3field-weighted citation impact, top 5% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

56 citing papers in PubMed, 105 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. The Intricacies of Renal Phosphate Reabsorption-An Overview.International journal of molecular sciences · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. PHEXGenes · 2022
    Article
  9. Kidney stone formation in a novel murine model of polycystic kidney disease.American journal of physiology. Renal physiology · 2022
    Article
  10. Antagonism Between PEDF and TGF-β Contributes to Type VI Osteogenesis Imperfecta Bone and Vascular Pathogenesis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Two NovelGenes · 2020
    Article
  16. Article
  17. Review
  18. Article
  19. Variants affecting diverse domains of MEPE are associated with two distinct bone disorders, a craniofacial bone defect and otosclerosis.Genetics in medicine : official journal of the American College of Medical Genetics · 2019
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Valentin DavidThe Kidney Institute, Kansas University Medical Center, Kansas City, Kansas 66160, USA.
Aline Martin
Anne-Marie Hedge
Peter S N Rowe
University of Kansas Medical Center · USUniversity Medical Center · US

Funding

Mineralization of the matrix in disease and healthR01AR051598 · NIAMS · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI ROWE, PETER S · 2004 to 2013
$2.8M
NIAMS NIH HHS R01 AR051598NIAMS NIH HHS R01AR051598
6 · The paper itself

Abstract

Increased matrix extracellular phosphoglycoprotein (MEPE) expression occurs in several phosphate and bone-mineral metabolic disorders. To resolve whether MEPE plays a role, we created a murine model overexpressing MEPE protein (MEPE tgn) in bone. MEPE tgn mice displayed a growth and mineralization defect with altered bone-renal vascularization that persisted to adulthood. The growth mineralization defect was due to a decrease in bone remodeling, and MEPE tgn mice were resistant to diet-induced renal calcification. MEPE protein-derived urinary ASARM peptides and reduced urinary Ca X PO4 product mediated the suppressed renal calcification. Osteoblastic cells displayed reduced activity but normal differentiation. Osteoclastic precursors were unable to differentiate in the presence of osteoblasts. In the kidney, NPT2a up-regulation induced an increase in phosphate renal reabsorption, leading to hyperphosphatemia. We conclude MEPE and MEPE-phosphate-regulating gene with homologies to endopeptidases on the X chromosome (MEPE-PHEX) interactions are components to an age-diet-dependent pathway that regulates bone turnover and mineralization and suppresses renal calcification. This novel pathway also modulates bone-renal vascularization and bone turnover.

Indexed as

AgingAldosteroneAnimal Nutritional Physiological PhenomenaAnimalsBone and BonesBone DevelopmentCalcitriolExtracellular Matrix ProteinsGlycoproteinsHyperphosphatemiaHypocalcemiaKidneyMiceMice, Inbred C57BLMice, TransgenicNeovascularization, PathologicAldosteroneCalcitriolExtracellular Matrix ProteinsGlycoproteinsMepe protein, mouseOsteopontinParathyroid HormonePHEX Phosphate Regulating Neutral EndopeptidasePhex protein, mousePhosphoproteinsSpp1 protein, mouseVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouse

Identifiers

PMID19520780
PMCPMC2819738
OpenAlexW2000443667

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.