Evidence map›Paper›PMID 23938401›Full record

ReviewFree radical biology & medicine2013

Implications of autophagy for vascular smooth muscle cell function and plasticity.

Joshua K Salabei, Bradford G Hill

Open access · greenAbstract readReview
In one paragraph

Review in Free radical biology & medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 6% 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

64 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Rosuvastatin activates autophagyThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Annals of translational medicine · 2023
    Article
  20. Review

4 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.

Joshua K SalabeiDiabetes and Obesity Center, Institute of Molecular Cardiology, University of Louisville School of Medicine, Louisville, KY 40202, USA.
Bradford G HillDiabetes and Obesity Center, Institute of Molecular Cardiology, University of Louisville School of Medicine, Louisville, KY 40202, USA; Department of Biochemistry and Molecular Biology, University of Louisville School of Medicine, Louisville, KY 40202, USA; Department of Physiology and Biophysics, University of Louisville School of Medicine, Louisville, KY 40202, USA. Electronic address: bradford.hill@louisville.edu.
University of Louisville · US

Funding

Project 5 - Metabolomic Analysis of AtherothrombosisP20GM103492 · NIGMS · UNIVERSITY OF LOUISVILLE · PI DEFILIPPIS, ANDREW · 2012 to 2017
$13.8M
STEM CELLS AND DIABETIC CARDIOMYOPATHY PROJ 2 2009P20RR024489 · NCRR · UNIVERSITY OF LOUISVILLE · PI BHATNAGAR, ARUNI · 2008 to 2011
$10.0M
NCRR NIH HHS P20 RR024489NIGMS NIH HHS GM103492NIGMS NIH HHS P20 GM103492
6 · The paper itself

Abstract

Vascular smooth muscle cells (VSMCs) are fundamental in regulating blood pressure and distributing oxygen and nutrients to peripheral tissues. They also possess remarkable plasticity, with the capacity to switch to synthetic, macrophage-like, or osteochondrogenic phenotypes when cued by external stimuli. In arterial diseases such as atherosclerosis and restenosis, this plasticity seems to be critical and, depending on the disease context, can be deleterious or beneficial. Therefore, understanding the mechanisms regulating VSMC phenotype and survival is essential for developing new therapies for vascular disease as well as understanding how secondary complications due to surgical interventions develop. In this regard, the cellular process of autophagy is increasingly being recognized as a major player in vascular biology and a critical determinant of VSMC phenotype and survival. Although autophagy was identified in lesional VSMCs in the 1960s, our understanding of the implications of autophagy in arterial diseases and the stimuli promoting its activation in VSMCs is only now being elucidated. In this review, we highlight the evidence for autophagy occurring in VSMCs in vivo, elaborate on the stimuli and processes regulating autophagy, and discuss the current understanding of the role of autophagy in vascular disease.

Indexed as

AnimalsAutophagyCell DedifferentiationHumansMuscle, Smooth, VascularAtherosclerosisCardiovascularFree radicalsHypertensionOxidative stressProliferationRestenosis

Identifiers

PMID23938401
PMCPMC3859773
OpenAlexW1974132613

What OpenQuestion 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 OpenQuestion graph.