Evidence map›Paper›PMID 30894089›Full record

ArticleCirculation research2019

Endothelial SIRT6 Is Vital to Prevent Hypertension and Associated Cardiorenal Injury Through Targeting Nkx3.2-GATA5 Signaling.

Jian Guo, Ziying Wang, Jichao Wu, Min Liu, Mengmeng Li, Yu Sun, Wei Huang, Yujia Li, Yan Zhang, Wei Tang and 6 more

Open access · bronzeAbstract read
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In one paragraph

Article in Circulation research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
8.9field-weighted citation impact, top 1% 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

93 citing papers in PubMed, 149 citations in OpenAlex.

  1. Article
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  16. Inhibition of AMPKα Pathway by Podocyte GOLM1 Exacerbates Diabetic Nephrology in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  17. Cellular senescence in kidney diseases.Chinese medical journal · 2025
    Review
  18. Review
  19. Review
  20. Article

33 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 4 institutions in 2 countries.

Jian GuoFrom the Key Laboratory of Infection and Immunity of Shandong Province, Department of Pharmacology (J.G., Z.W., J.W., M. Liu, W.H., Y.L., Y.Z., F.Y.), Shandong University, Jinan, China.
Ziying WangFrom the Key Laboratory of Infection and Immunity of Shandong Province, Department of Pharmacology (J.G., Z.W., J.W., M. Liu, W.H., Y.L., Y.Z., F.Y.), Shandong University, Jinan, China.
Jichao WuFrom the Key Laboratory of Infection and Immunity of Shandong Province, Department of Pharmacology (J.G., Z.W., J.W., M. Liu, W.H., Y.L., Y.Z., F.Y.), Shandong University, Jinan, China.
Min LiuFrom the Key Laboratory of Infection and Immunity of Shandong Province, Department of Pharmacology (J.G., Z.W., J.W., M. Liu, W.H., Y.L., Y.Z., F.Y.), Shandong University, Jinan, China.
Mengmeng LiSchool of Basic Medical Science, The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Qilu Hospital (M. Li), Shandong University, Jinan, China.
Yu SunFrom the Key Laboratory of Infection and Immunity of Shandong Province, Department of Pharmacology (J.G., Z.W., J.W., M. Liu, W.H., Y.L., Y.Z., F.Y.), Shandong University, Jinan, China.
Wei HuangFrom the Key Laboratory of Infection and Immunity of Shandong Province, Department of Pharmacology (J.G., Z.W., J.W., M. Liu, W.H., Y.L., Y.Z., F.Y.), Shandong University, Jinan, China.
Yujia LiFrom the Key Laboratory of Infection and Immunity of Shandong Province, Department of Pharmacology (J.G., Z.W., J.W., M. Liu, W.H., Y.L., Y.Z., F.Y.), Shandong University, Jinan, China.
Yan ZhangFrom the Key Laboratory of Infection and Immunity of Shandong Province, Department of Pharmacology (J.G., Z.W., J.W., M. Liu, W.H., Y.L., Y.Z., F.Y.), Shandong University, Jinan, China.
Wei TangDepartment of Pathogenic Biology, School of Basic Medical Science (W.T.), Shandong University, Jinan, China.
Xiaoyan LiShandong Provincial Key Laboratory of Oral Biomedicine, Department of Endodontics, School of Stomatology (X.L.), Shandong University, Jinan, China.
Chun ZhangDepartment of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China (C.Z.).
Fanzhen HongDepartment of Obstetrics and Gynecology, Second Hospital of Shandong University, Jinan, China (F.H.).
Ningjun LiDepartment of Pharmacology and Toxicology, Medical College of Virginia, Virginia Commonwealth University, Richmond (N.L.).
Jing NieState Key Laboratory of Organ Failure Research, National Clinical Research Center of Kidney Disease, Key Laboratory of Organ Failure Research (Ministry of Education), Division of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, China (J.N.).
Fan YiFrom the Key Laboratory of Infection and Immunity of Shandong Province, Department of Pharmacology (J.G., Z.W., J.W., M. Liu, W.H., Y.L., Y.Z., F.Y.), Shandong University, Jinan, China.
Shandong University · CNSecond Hospital of Shandong University · CNUnion Hospital · CNVirginia Commonwealth University Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

rationaleEndothelial dysfunction is an important determinant risk factor for the development of hypertension and its complications. Thus, identification of potential therapeutic targets for preventing endothelial dysfunction has major clinical importance. Emerging evidence indicates that epigenetic modifications are closely associated with the regulation of endothelial function. Among them, HDAC (histone deacetylase)-mediated epigenetic processes in vascular homeostasis and cardiovascular disease have attracted much attention. SIRT6 (sirtuin 6) is one member of SIRTs (class III HDAC) that are highly conserved NAD

objectiveThis study was designed to elucidate the role of SIRT6 in the pathogenesis of hypertension, discover the new targets of SIRT6, and explore related mechanisms on the regulation of endothelial function. METHODS AND

resultsThe levels of endothelial SIRT6 were significantly reduced in 2 independent hypertension models: desoxycorticosterone acetate/salt-induced and Ang II (angiotensin II)-induced hypertensive mice. Utilizing genetically engineered endothelial-specific SIRT6 knockout (Cre

conclusionsThis study for the first time demonstrates that SIRT6 prevents hypertension and its complications by maintaining endothelial function. Pharmacological targeting of SIRT6 may be an innovative therapeutic strategy for treating patients with hypertension.

Indexed as

AcetylationAngiotensin IIAnimalsDesoxycorticosterone AcetateEndothelium, VascularEpigenesis, GeneticGATA5 Transcription FactorHistone DeacetylasesHistonesHomeodomain ProteinsHypertensionHypertension, RenalKidneyMiceMice, KnockoutNephritisAngiotensin IIDesoxycorticosterone AcetateGata5 protein, mouseGATA5 Transcription FactorHistone DeacetylasesHistonesHomeodomain ProteinsNkx3-2 protein, mouseSirt6 protein, mouseSirtuinsSodium ChlorideTranscription FactorsVasoconstrictor Agentsangiotensinautophagyendotheliumhistonehypertensionnitric oxide

Identifiers

PMID30894089
OpenAlexW2924884438

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.