Evidence map›Paper›PMID 32111067›Full record

ReviewInternational journal of molecular sciences2020

Sirtuin-1 and Its Relevance in Vascular Calcification.

Chien-Lin Lu, Min-Tser Liao, Yi-Chou Hou, Yu-Wei Fang, Cai-Mei Zheng, Wen-Chih Liu, Chia-Ter Chao, Kuo-Cheng Lu, Yee-Yung Ng

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.5field-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

38 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Review
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  5. Liuwei Dihuang Prevents Human Umbilical Vein Endothelial Cells SenescenceCombinatorial chemistry & high throughput screening · 2026
    Article
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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

9 authors at 4 institutions in 1 country.

Chien-Lin LuDivision of Nephrology, Department of Medicine, Fu Jen Catholic University Hospital, School of Medicine, Fu Jen Catholic University, New Taipei City 242, Taiwan.ORCID 0000-0002-9452-5179
Min-Tser LiaoDepartment of Pediatrics, Taoyuan Armed Forces General Hospital, Taoyuan City 325, Taiwan.
Yi-Chou HouSchool of Medicine, College of Medicine, Fu-Jen Catholic University, New Taipei City 24205, Taiwan.
Yu-Wei FangSchool of Medicine, College of Medicine, Fu-Jen Catholic University, New Taipei City 24205, Taiwan.
Cai-Mei ZhengGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei 110, Taiwan.ORCID 0000-0003-0370-3951
Wen-Chih LiuGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei 110, Taiwan.
Chia-Ter ChaoGraduate Institute of Toxicology, National Taiwan University College of Medicine, Taipei 104, Taiwan.
Kuo-Cheng LuDivision of Nephrology, Department of Medicine, Fu Jen Catholic University Hospital, School of Medicine, Fu Jen Catholic University, New Taipei City 242, Taiwan.
Yee-Yung NgDivision of Nephrology, Department of Medicine, Fu Jen Catholic University Hospital, School of Medicine, Fu Jen Catholic University, New Taipei City 242, Taiwan.
Fu Jen Catholic University · TWNational Taiwan University · TWTaipei Medical University-Shuang Ho Hospital · TWTungs' Taichung MetroHarbor Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular calcification (VC) is highly associated with cardiovascular disease and all-cause mortality in patients with chronic kidney disease. Dysregulation of endothelial cells and vascular smooth muscle cells (VSMCs) is related to VC. Sirtuin-1 (Sirt1) deacetylase encompasses a broad range of transcription factors that are linked to an extended lifespan. Sirt1 enhances endothelial NO synthase and upregulates FoxOs to activate its antioxidant properties and delay cell senescence. Sirt1 reverses osteogenic phenotypic transdifferentiation by influencing RUNX2 expression in VSMCs. Low Sirt1 hardly prevents acetylation by p300 and phosphorylation of β-catenin that, following the facilitation of β-catenin translocation, drives osteogenic phenotypic transdifferentiation. Hyperphosphatemia induces VC by osteogenic conversion, apoptosis, and senescence of VSMCs through the Pit-1 cotransporter, which can be retarded by the sirt1 activator resveratrol. Proinflammatory adipocytokines released from dysfunctional perivascular adipose tissue (PVAT) mediate medial calcification and arterial stiffness. Sirt1 ameliorates release of PVAT adipokines and increases adiponectin secretion, which interact with FoxO 1 against oxidative stress and inflammatory arterial insult. Conclusively, Sirt1 decelerates VC by means of influencing endothelial NO bioavailability, senescence of ECs and VSMCs, osteogenic phenotypic transdifferentiation, apoptosis of VSMCs, ECM deposition, and the inflammatory response of PVAT. Factors that aggravate VC include vitamin D deficiency-related macrophage recruitment and further inflammation responses. Supplementation with vitamin D to adequate levels is beneficial in improving PVAT macrophage infiltration and local inflammation, which further prevents VC.

Indexed as

AdipokinesAdipose TissueAnimalsApoptosisbeta CateninCardiovascular DiseasesCell TransdifferentiationEndothelial CellsForkhead Box Protein O1HumansMyocytes, Smooth MuscleNitric OxideOsteogenesisSirtuin 1Transcription FactorsVascular CalcificationAdipokinesbeta CateninForkhead Box Protein O1Nitric OxideSirtuin 1Transcription Factorsendothelial cellsperivascular adipose tissuesirtuin-1vascular calcificationvascular smooth muscle cells

Identifiers

PMID32111067
PMCPMC7084838
OpenAlexW3007313106

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.