Evidence map›Paper›PMID 28992202›Full record

ReviewJournal of molecular cell biology2017

Krüppel-like factors and vascular wall homeostasis.

Yanbo Fan, Haocheng Lu, Wenying Liang, Wenting Hu, Jifeng Zhang, Y Eugene Chen

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of molecular cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
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

67 citing papers in PubMed, 128 citations in OpenAlex.

  1. Review
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  6. Review
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  9. Review
  10. Phenotypic Switching of VSMCs in the Development of CVDs: Focus on miRs.International journal of molecular sciences · 2025
    Review
  11. Article
  12. Fluid Shear Stress-Regulated Vascular Remodeling: Past, Present, and Future.Arteriosclerosis, thrombosis, and vascular biology · 2025
    Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
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  20. Review

7 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

6 authors at 1 institution in 1 country.

Yanbo FanCardiovascular Center, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI, USA.
Haocheng LuCardiovascular Center, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI, USA.
Wenying LiangCardiovascular Center, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI, USA.
Wenting HuCardiovascular Center, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI, USA.
Jifeng ZhangCardiovascular Center, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI, USA.
Y Eugene ChenCardiovascular Center, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI, USA.
University of Michigan–Ann Arbor · US

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
Kruppel-like factor 11 (KLF11) and atherosclerosisR01HL138139 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ZHANG, JIFENG · 2017 to 2021
$2.3M
NHLBI NIH HHS R01 HL138139NIDDK NIH HHS P30 DK020572
6 · The paper itself

Abstract

Cardiovascular diseases (CVDs) are major causes of death worldwide. Identification of promising targets for prevention and treatment of CVDs is paramount in the cardiovascular field. Numerous transcription factors regulate cellular function through modulation of specific genes and thereby are involved in the physiological and pathophysiological processes of CVDs. Although Krüppel-like factors (KLFs) have a similar protein structure with a conserved zinc finger domain, they possess distinct tissue and cell distribution patterns as well as biological functions. In the vascular system, KLF activities are regulated at both transcriptional and posttranscriptional levels. Growing in vitro, in vivo, and genetic epidemiology studies suggest that specific KLFs play important roles in vascular wall biology, which further affect vascular diseases. KLFs regulate various functional aspects such as cell growth, differentiation, activation, and development through controlling a whole cluster of functionally related genes and modulating various signaling pathways in response to pathological conditions. Therapeutic targeting of selective KLF family members may be desirable to achieve distinct treatment effects in the context of various vascular diseases. Further elucidation of the association of KLFs with human CVDs, their underlying molecular mechanisms, and precise protein structure studies will be essential to define KLFs as promising targets for therapeutic interventions in CVDs.

Indexed as

HomeostasisAnimalsBlood VesselsCardiovascular DiseasesDisease SusceptibilityEndothelial CellsGene Expression RegulationHemodynamicsHumansKruppel-Like Transcription FactorsModels, BiologicalMultigene FamilyMyocytes, Smooth MuscleNeovascularization, PathologicNeovascularization, PhysiologicSignal TransductionKruppel-Like Transcription Factorsatherosclerosisdrug developmentendothelial cellsinflammationshear stressvascular injuryvascular smooth muscle cells

Identifiers

PMID28992202
PMCPMC5907833
OpenAlexW2745487428

What OpenQuestion holds

Textmetadata
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.