Evidence map›Paper›PMID 25908728›Full record

ReviewCirculation research2015

The genetic basis of peripheral arterial disease: current knowledge, challenges, and future directions.

Iftikhar J Kullo, Nicholas J Leeper

Open access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 4% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Guideline
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. miRNA-6236 Regulation of Postischemic Skeletal Muscle Angiogenesis.Journal of the American Heart Association · 2024
    Article
  11. Review
  12. Article
  13. Sex and Racial Disparities in Peripheral Artery Disease.Arteriosclerosis, thrombosis, and vascular biology · 2023
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Genome-Wide Association Study of Peripheral Artery Disease.Circulation. Genomic and precision medicine · 2021
    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

2 authors at 1 institution in 1 country.

Iftikhar J KulloFrom the Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN (I.J.K.); and Department of Vascular Surgery, Stanford, Stanford, CA (N.J.L.). kullo.iftikhar@mayo.edu.
Nicholas J LeeperFrom the Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN (I.J.K.); and Department of Vascular Surgery, Stanford, Stanford, CA (N.J.L.).
Mayo Clinic in Arizona · US

Funding

Genomic Basis of Susceptibility to COVID-19 Infection and its ComplicationsU01HG006379 · NHGRI · MAYO CLINIC ROCHESTER · PI Richard R. Sharp · 2011 to 2026
$16.5M
The paradoxical role of CDKN2B in blood vessel sprouting and maturationR01HL125224 · NHLBI · STANFORD UNIVERSITY · PI LEEPER, NICHOLAS JAMES · 2015 to 2018
$1.9M
The role of CDKN2B in AAA diseaseK08HL103605 · NHLBI · STANFORD UNIVERSITY · PI LEEPER, NICHOLAS JAMES · 2012 to 2014
$400k
NHGRI NIH HHS U01 HG006379NHGRI NIH HHS U01HG006379NHLBI NIH HHS K08 HL103605NHLBI NIH HHS K08HL10360503NHLBI NIH HHS R01 HL125224NHLBI NIH HHS R01HL125224
6 · The paper itself

Abstract

Several risk factors for atherosclerotic peripheral arterial disease (PAD), such as dyslipidemia, diabetes mellitus, and hypertension, are heritable. However, predisposition to PAD may be influenced by genetic variants acting independently of these risk factors. Identification of such genetic variants will provide insights into underlying pathophysiologic mechanisms and facilitate the development of novel diagnostic and therapeutic approaches. In contrast to coronary heart disease, relatively few genetic variants that influence susceptibility to PAD have been discovered. This may be, in part, because of greater clinical and genetic heterogeneity in PAD. In this review, we (1) provide an update on the current state of knowledge about the genetic basis of PAD, including results of family studies and candidate gene, linkage as well as genome-wide association studies; (2) highlight the challenges in investigating the genetic basis of PAD and possible strategies to overcome these challenges; and (3) discuss the potential of genome sequencing, RNA sequencing, differential gene expression, epigenetic profiling, and systems biology in increasing our understanding of the molecular genetics of PAD.

Indexed as

Polymorphism, Single NucleotideEpigenesis, GeneticForecastingGene-Environment InteractionGene Expression ProfilingGenetic Predisposition to DiseaseGenome-Wide Association StudyHigh-Throughput Nucleotide SequencingHumansPeripheral Arterial Diseaseepigenomicsgenome-wide association studymolecular epidemiologyperipheral arterial disease

Identifiers

PMID25908728
PMCPMC4410432
OpenAlexW2146704860

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.