Evidence map›Paper›PMID 30602303›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2019

KLF11 (Krüppel-Like Factor 11) Inhibits Arterial Thrombosis via Suppression of Tissue Factor in the Vascular Wall.

Wenying Liang, Yanbo Fan, Haocheng Lu, Ziyi Chang, Wenting Hu, Jinjian Sun, Huilun Wang, Tianqing Zhu, Jintao Wang, Reheman Adili and 5 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. TGF-β and TNF-α Signaling Crosstalk in Human Coronary Artery Cells.International journal of molecular sciences · 2026
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  15. Recent Insights Into the Regulation of Coagulation and Thrombosis.Arteriosclerosis, thrombosis, and vascular biology · 2020
    Review
  16. KLF11 (Krüppel-Like Factor 11) Modulates Arterial Thrombosis.Arteriosclerosis, thrombosis, and vascular biology · 2019
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 1 institution in 1 country.

Wenying LiangFrom the Department of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor (W.L., Y.F., H.L., Z.C., W.H., J.S., H.W., T.Z., J.W., M.T.G.-B., D.E., J.Z., Y.E.C.).
Yanbo FanFrom the Department of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor (W.L., Y.F., H.L., Z.C., W.H., J.S., H.W., T.Z., J.W., M.T.G.-B., D.E., J.Z., Y.E.C.).
Haocheng LuFrom the Department of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor (W.L., Y.F., H.L., Z.C., W.H., J.S., H.W., T.Z., J.W., M.T.G.-B., D.E., J.Z., Y.E.C.).
Ziyi ChangFrom the Department of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor (W.L., Y.F., H.L., Z.C., W.H., J.S., H.W., T.Z., J.W., M.T.G.-B., D.E., J.Z., Y.E.C.).
Wenting HuFrom the Department of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor (W.L., Y.F., H.L., Z.C., W.H., J.S., H.W., T.Z., J.W., M.T.G.-B., D.E., J.Z., Y.E.C.).
Jinjian SunFrom the Department of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor (W.L., Y.F., H.L., Z.C., W.H., J.S., H.W., T.Z., J.W., M.T.G.-B., D.E., J.Z., Y.E.C.).
Huilun WangFrom the Department of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor (W.L., Y.F., H.L., Z.C., W.H., J.S., H.W., T.Z., J.W., M.T.G.-B., D.E., J.Z., Y.E.C.).
Tianqing ZhuFrom the Department of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor (W.L., Y.F., H.L., Z.C., W.H., J.S., H.W., T.Z., J.W., M.T.G.-B., D.E., J.Z., Y.E.C.).
Jintao WangFrom the Department of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor (W.L., Y.F., H.L., Z.C., W.H., J.S., H.W., T.Z., J.W., M.T.G.-B., D.E., J.Z., Y.E.C.).
Reheman AdiliDepartment of Pharmacology, University of Michigan, Ann Arbor (R.A., M.H.).
Minerva T Garcia-BarrioFrom the Department of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor (W.L., Y.F., H.L., Z.C., W.H., J.S., H.W., T.Z., J.W., M.T.G.-B., D.E., J.Z., Y.E.C.).
Michael HolinstatDepartment of Pharmacology, University of Michigan, Ann Arbor (R.A., M.H.).
Daniel EitzmanFrom the Department of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor (W.L., Y.F., H.L., Z.C., W.H., J.S., H.W., T.Z., J.W., M.T.G.-B., D.E., J.Z., Y.E.C.).
Jifeng ZhangFrom the Department of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor (W.L., Y.F., H.L., Z.C., W.H., J.S., H.W., T.Z., J.W., M.T.G.-B., D.E., J.Z., Y.E.C.).
Y Eugene ChenFrom the Department of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor (W.L., Y.F., H.L., Z.C., W.H., J.S., H.W., T.Z., J.W., M.T.G.-B., D.E., J.Z., Y.E.C.).
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
The Role of PPAR-gamma in Vascular Lesion FormationR01HL068878 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2002 to 2019
$7.6M
KLF14 and Cardiovascular DiseaseR01HL134569 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2017 to 2024
$5.3M
Two-stage miRNA delivering scaffolds for patient-originated cells to regenerate blood vesselsR01HL136231 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2017 to 2020
$3.0M
Kruppel-like factor 11 (KLF11) and atherosclerosisR01HL138139 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ZHANG, JIFENG · 2017 to 2021
$2.3M
The Role of TM6SF2 in Cardiovascular DiseaseR01HL137214 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2017 to 2020
$2.2M
Transcription Factor-EB and Postischemic AngiogenesisR01HL138094 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FAN, YANBO · 2017 to 2021
$2.2M
NHLBI NIH HHS R01 HL068878NHLBI NIH HHS R01 HL134569NHLBI NIH HHS R01 HL136231NHLBI NIH HHS R01 HL137214NHLBI NIH HHS R01 HL138094NHLBI NIH HHS R01 HL138139NIDDK NIH HHS P30 DK020572
6 · The paper itself

Abstract

Objective- Mutations in Krüppel like factor-11 ( KLF11), a gene also known as maturity-onset diabetes mellitus of the young type 7, contribute to the development of diabetes mellitus. KLF11 has anti-inflammatory effects in endothelial cells and beneficial effects on stroke. However, the function of KLF11 in the cardiovascular system is not fully unraveled. In this study, we investigated the role of KLF11 in vascular smooth muscle cell biology and arterial thrombosis. Approach and Results- Using a ferric chloride-induced thrombosis model, we found that the occlusion time was significantly reduced in conventional Klf11 knockout mice, whereas bone marrow transplantation could not rescue this phenotype, suggesting that vascular KLF11 is critical for inhibition of arterial thrombosis. We further demonstrated that vascular smooth muscle cell-specific Klf11 knockout mice also exhibited significantly reduced occlusion time. The expression of tissue factor (encoded by the F3 gene), a main initiator of the coagulation cascade, was increased in the artery of Klf11 knockout mice, as determined by real-time quantitative polymerase chain reaction and immunofluorescence. Furthermore, vascular smooth muscle cells isolated from Klf11 knockout mouse aortas showed increased tissue factor expression, which was rescued by KLF11 overexpression. In human aortic smooth muscle cells, small interfering RNA-mediated knockdown of KLF11 increased tissue factor expression. Consistent results were observed on adenovirus-mediated overexpression of KLF11. Mechanistically, KLF11 downregulates F3 at the transcriptional level as determined by reporter and chromatin immunoprecipitation assays. Conclusions- Our data demonstrate that KLF11 is a novel transcriptional suppressor of F3 in vascular smooth muscle cells, constituting a potential molecular target for inhibition of arterial thrombosis.

Indexed as

AnimalsAntithrombin IIIApoptosis Regulatory ProteinsBone Marrow TransplantationCells, CulturedChloridesChromatin ImmunoprecipitationDown-RegulationFemaleFerric CompoundsGene Expression RegulationHumansMaleMiceMice, Inbred C57BLMice, KnockoutAntithrombin IIIantithrombin III-protease complexApoptosis Regulatory ProteinsChloridesferric chlorideFerric CompoundsKLF11 protein, humanKLF11 protein, mousePeptide HydrolasesRecombinant ProteinsRepressor ProteinsThromboplastindiabetes mellitusgeneKrüppel-like factorsthrombosistissue factorvascular disease

Identifiers

PMID30602303
PMCPMC6393209
OpenAlexW2908456598

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.