Evidence map›Paper›PMID 25544597›Full record

ReviewRedox biology2015

Autophagic regulation of smooth muscle cell biology.

Joshua K Salabei, Bradford G Hill

Open access · goldAbstract readReview
In one paragraph

Review in Redox biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.7field-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

42 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
  2. Rosuvastatin activates autophagyThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Lactate promotes vascular smooth muscle cell switch to a synthetic phenotype by inhibiting miR-23b expression.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Vasculoprotective effects ofJournal of traditional and complementary medicine · 2020
    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.

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

Funding

Tumor Necrosis Factor Modulation of CPCsP01HL078825 · NHLBI · UNIVERSITY OF LOUISVILLE · PI BOLLI, ROBERTO · 2005 to 2021
$37.6M
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 RR024489NHLBI NIH HHS HL78825NHLBI NIH HHS P01 HL078825NIGMS NIH HHS GM103492NIGMS NIH HHS P20 GM103492
6 · The paper itself

Abstract

Autophagy regulates the metabolism, survival, and function of numerous cell types, including those comprising the cardiovascular system. In the vasculature, changes in autophagy have been documented in atherosclerotic and restenotic lesions and in hypertensive vessels. The biology of vascular smooth muscle cells appears particularly sensitive to changes in the autophagic program. Recent evidence indicates that stimuli or stressors evoked during the course of vascular disease can regulate autophagic activity, resulting in modulation of VSMC phenotype and viability. In particular, certain growth factors and cytokines, oxygen tension, and pharmacological drugs have been shown to trigger autophagy in smooth muscle cells. Importantly, each of these stimuli has a redox component, typically associated with changes in the abundance of reactive oxygen, nitrogen, or lipid species. Collective findings support the hypothesis that autophagy plays a critical role in vascular remodeling by regulating smooth muscle cell phenotype transitions and by influencing the cellular response to stress. In this graphical review, we summarize current knowledge on the role of autophagy in the biology of the smooth muscle cell in (patho)physiology.

Indexed as

AtherosclerosisAutophagyHumansLipid MetabolismMuscle, Smooth, VascularMyocytes, Smooth MuscleOxidative StressAtherosclerosisAutophagyMetabolismOxidative stressPlatelet-derived growth factorRestenosis

Identifiers

PMID25544597
PMCPMC4309847
OpenAlexW2021822355

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.