Evidence map›Paper›PMID 26675253›Full record

ArticleJournal of the American Heart Association2015

Transgenic Overexpression of Tissue-Nonspecific Alkaline Phosphatase (TNAP) in Vascular Endothelium Results in Generalized Arterial Calcification.

Alexei Y Savinov, Maryam Salehi, Manisha C Yadav, Ilian Radichev, José Luis Millán, Olga V Savinova

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2015. 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
3.1field-weighted citation impact, top 9% 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, 89 citations in OpenAlex.

  1. Article
  2. ENPP1 inhibition as a therapeutic approach for later-onset hypophosphatasia.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2026
    Article
  3. Hypophosphatasia-pathophysiological understanding, preclinical data looking beyond the skeleton, and upcoming treatments.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2026
    Review
  4. Review
  5. Atherosclerosis: A Pathologist's Perspective.Journal of cardiovascular development and disease · 2026
    Review
  6. Article
  7. Soft tissue calcifications in chronic kidney disease-beyond the vasculature.Pflugers Archiv : European journal of physiology · 2025
    Review
  8. Review
  9. Considerations on the Development of Therapeutics in Vascular Calcification.Journal of cardiovascular development and disease · 2025
    Review
  10. Atherosclerosis: A Comprehensive Review of Molecular Factors and Mechanisms.International journal of molecular sciences · 2025
    Review
  11. Article
  12. Weighing the Evidence for the Roles of Plasma Versus Local Pyrophosphate in Ectopic Calcification Disorders.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
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

6 authors at 4 institutions in 1 country.

Alexei Y SavinovChildren's Health Research Center, Sanford Research, Sioux Falls, SD (A.Y.S., M.S., I.R., O.V.S.) Department of Pediatrics, Sanford School of Medicine, University of South Dakota, Sioux Falls, SD (A.Y.S.).
Maryam SalehiChildren's Health Research Center, Sanford Research, Sioux Falls, SD (A.Y.S., M.S., I.R., O.V.S.) Division of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, SD (M.S.).
Manisha C YadavSanford Children's Health Research Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA (M.C.Y., J.L.M.).
Ilian RadichevChildren's Health Research Center, Sanford Research, Sioux Falls, SD (A.Y.S., M.S., I.R., O.V.S.).
José Luis MillánSanford Children's Health Research Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA (M.C.Y., J.L.M.).
Olga V SavinovaChildren's Health Research Center, Sanford Research, Sioux Falls, SD (A.Y.S., M.S., I.R., O.V.S.).
Sanford Research · USUniversity of South Dakota · USDiscovery Institute · USSanford Burnham Prebys Medical Discovery Institute · US

Funding

Yeast 2 HybridP20GM103620 · NIGMS · SANFORD RESEARCH/USD · PI ROUX, KYLE J · 2013 to 2023
$24.2M
MOLECULAR PATHOGENESIS/TREATMENT OF HYPOPHOSPHATASIAR01DE012889 · NIDCR · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI MILLAN, JOSE LUIS · 1999 to 2020
$9.2M
Genetic Regulation of Human Beta Cell DestructionUC4DK104194 · NIDDK · UNIVERSITY OF FLORIDA · PI MATHEWS, CLAYTON E · 2014 to 2014
$3.1M
NIDCR NIH HHS DE12889NIDCR NIH HHS R01 DE012889NIDDK NIH HHS UC4 DK104194NIGMS NIH HHS P20 GM103620
6 · The paper itself

Abstract

backgroundEctopic vascular calcification is a common condition associated with aging, atherosclerosis, diabetes, and/or chronic kidney disease. Smooth muscle cells are the best characterized source of osteogenic progenitors in the vasculature; however, recent studies suggest that cells of endothelial origin can also promote calcification. To test this, we sought to increase the osteogenic potential of endothelial cells by overexpressing tissue-nonspecific alkaline phosphatase (TNAP), a key enzyme that regulates biomineralization, and to determine the pathophysiological effect of endothelial TNAP on vascular calcification and cardiovascular function. METHODS AND

resultsWe demonstrated previously that mice transgenic for ALPL (gene encoding human TNAP) develop severe arterial medial calcification and reduced viability when TNAP is overexpressed in smooth muscle cells. In this study, we expressed the ALPL transgene in endothelial cells following endothelial-specific Tie2-Cre recombination. Mice with endothelial TNAP overexpression survived well into adulthood and displayed generalized arterial calcification. Genes associated with osteochondrogenesis (Runx2, Bglap, Spp1, Opg, and Col2a1) were upregulated in the aortas of endothelial TNAP animals compared with controls. Lesions in coronary arteries of endothelial TNAP mice showed immunoreactivity to Runx2, osteocalcin, osteopontin, and collagen II as well as increased deposition of sialoproteins revealed by lectin staining. By 23 weeks of age, endothelial TNAP mice developed elevated blood pressure and compensatory left ventricular hypertrophy with preserved ejection fraction.

conclusionsThis study presented a novel genetic model demonstrating the osteogenic potential of TNAP-positive endothelial cells in promoting pathophysiological vascular calcification.

Indexed as

Alkaline PhosphataseAnimalsCalcinosisEndothelium, VascularFemaleGene ExpressionMaleMiceMice, TransgenicPeripheral Arterial DiseaseReal-Time Polymerase Chain ReactionAlkaline PhosphataseALPL protein, mousearteriosclerosiscardiovascular diseasesendotheliumenzymeslesion

Identifiers

PMID26675253
PMCPMC4845279
OpenAlexW2208579015

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.