Evidence map›Paper›PMID 28062508›Full record

ReviewArteriosclerosis, thrombosis, and vascular biology2017

Arterial Calcification in Diabetes Mellitus: Preclinical Models and Translational Implications.

John N Stabley, Dwight A Towler

Open access · bronzeAbstract readReview
In one paragraph

Review in Arteriosclerosis, thrombosis, and vascular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
10.8field-weighted citation impact, top 2% 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

71 citing papers in PubMed, 143 citations in OpenAlex.

  1. Article
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  4. Article
  5. Review
  6. Iron in Vascular Calcification: Pro-Calcific Agent or Protective Modulator?International journal of molecular sciences · 2025
    Review
  7. Article
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  12. Review
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  18. Article
  19. Vascular frailty, a proposal for new frailty type: A narrative review.The Kaohsiung journal of medical sciences · 2023
    Review
  20. Review

11 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

John N StableyFrom the Division of Endocrinology, Department of Internal Medicine, UT Southwestern Medical Center, Dallas, TX.
Dwight A TowlerFrom the Division of Endocrinology, Department of Internal Medicine, UT Southwestern Medical Center, Dallas, TX. dwight.towler@utsouthwestern.edu.
Southwestern Medical Center · US

Funding

OSTEOGENIC REGULATION OF VASCULAR CALCIFICATIONR01HL069229 · NHLBI · WASHINGTON UNIVERSITY · PI TOWLER, DWIGHT A. · 2001 to 2022
$7.9M
Endocrine Regulation of Calcific Aortic Valve Sclerosis: PTH/PTHRP Receptor SignaR01HL114806 · NHLBI · WASHINGTON UNIVERSITY · PI TOWLER, DWIGHT A. · 2012 to 2016
$2.1M
NHLBI NIH HHS R01 HL069229NHLBI NIH HHS R01 HL114806
6 · The paper itself

Abstract

Diabetes mellitus increasingly afflicts our aging and dysmetabolic population. Type 2 diabetes mellitus and the antecedent metabolic syndrome represent the vast majority of the disease burden-increasingly prevalent in children and older adults. However, type 1 diabetes mellitus is also advancing in preadolescent children. As such, a crushing wave of cardiometabolic disease burden now faces our society. Arteriosclerotic calcification is increased in metabolic syndrome, type 2 diabetes mellitus, and type 1 diabetes mellitus-impairing conduit vessel compliance and function, thereby increasing the risk for dementia, stroke, heart attack, limb ischemia, renal insufficiency, and lower extremity amputation. Preclinical models of these dysmetabolic settings have provided insights into the pathobiology of arterial calcification. Osteochondrogenic morphogens in the BMP-Wnt signaling relay and transcriptional regulatory programs driven by Msx and Runx gene families are entrained to innate immune responses-responses activated by the dysmetabolic state-to direct arterial matrix deposition and mineralization. Recent studies implicate the endothelial-mesenchymal transition in contributing to the phenotypic drift of mineralizing vascular progenitors. In this brief overview, we discuss preclinical disease models that provide mechanistic insights-and point to challenges and opportunities to translate these insights into new therapeutic strategies for our patients afflicted with diabetes mellitus and its arteriosclerotic complications.

Indexed as

Translational Research, BiomedicalAnimalsAnimals, Genetically ModifiedArteriesAtherosclerosisDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2Diabetic AngiopathiesDiet, High-FatDisease Models, AnimalFemaleGenetic Predisposition to DiseaseHumansHyperlipidemiasMaleamputationarteriosclerosisdementiadiabetes mellitusvascular calcification

Identifiers

PMID28062508
PMCPMC5480317
OpenAlexW2563577205

What Socratic holds

Textmetadata
LicenceTDM
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.