Evidence map›Paper›PMID 35396645›Full record

ArticleInternational urology and nephrology2022

Both high glucose and phosphate overload promote senescence-associated calcification of vascular muscle cells.

Mingming Zhang, Tianyu Li, Zhenzhen Tu, Yuying Zhang, Xuerong Wang, Dandan Zang, Deping Xu, Yang Feng, Fan He, Mingyue Ni and 2 more

Abstract read
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In one paragraph

Article in International urology and nephrology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

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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

12 authors at 1 institution in 1 country.

Mingming ZhangDepartment of Nephrology, The Second Affiliated Hospital of Anhui Medical University, Hefei, China.ORCID http://orcid.org/0000-0002-6288-0918
Tianyu LiDepartment of Nephrology, The Second Affiliated Hospital of Anhui Medical University, Hefei, China.
Zhenzhen TuDepartment of Biochemistry and Molecular Biology, Anhui Medical University, Hefei, China.
Yuying ZhangDepartment of Nephrology, The Second Affiliated Hospital of Anhui Medical University, Hefei, China.
Xuerong WangDepartment of Nephrology, The Second Affiliated Hospital of Anhui Medical University, Hefei, China.
Dandan ZangThe Center for Scientific Research of Anhui Medical University, Hefei, China.
Deping XuDepartment of Clinical Laboratory, Affiliated Hefei Hospital of Anhui Medical University, Hefei, China.
Yang FengDepartment of Biochemistry and Molecular Biology, Anhui Medical University, Hefei, China.
Fan HeDepartment of Biochemistry and Molecular Biology, Anhui Medical University, Hefei, China.
Mingyue NiDepartment of Biochemistry and Molecular Biology, Anhui Medical University, Hefei, China.
Deguang WangDepartment of Nephrology, The Second Affiliated Hospital of Anhui Medical University, Hefei, China. wangdeguang@ahmu.edu.cn.
Haisheng ZhouDepartment of Biochemistry and Molecular Biology, Anhui Medical University, Hefei, China.
Anhui Medical University · CN

Funding

natural science foundation of anhui province 2008085MH244
6 · The paper itself

Abstract

purposeThe NAD

methodsVascular smooth muscle cells (VSMCs) were cultured under normal, high phosphate, and/or high-glucose conditions for 9 days. Alizarin red staining and calcification content analyses were used to determine calcium deposition. VSMC senescence was detected by β-galactosidase (SA-β-Gal) staining and p21 expression.

resultsMouse VSMCs exposed to high phosphate and high glucose in vitro showed increased calcification, which was correlated with the induction of cell senescence, as confirmed by the increased SA-β-galactosidase activity and p21 expression. SRT1720, an activator of SIRT1, inhibits p65 acetylation, the nuclear factor-κ-gene binding (NF-κB) pathway, and VSMC transdifferentiation, prevents senescence and reactive oxygen species (ROS) production, and reduces vascular calcification. In contrast, sirtinol, an inhibitor of SIRT1, increases p65 acetylation, activates the NF-κB pathway, induces vascular smooth muscle cell transdifferentiation and senescence, and promotes vascular calcification.

conclusionsHigh glucose and high phosphate levels induce senescence and vascular calcification in VSMCs, and the combined effect of high glucose and phosphate can inhibit SIRT1 expression. SIRT1 inhibits vascular smooth muscle cell senescence and osteogenic differentiation by inhibiting NF-κB activity, thereby inhibiting vascular calcification.

Indexed as

Muscle, Smooth, VascularVascular CalcificationAnimalsbeta-GalactosidaseCells, CulturedGlucoseMiceMyocytes, Smooth MuscleNF-kappa BOsteogenesisPhosphatesSirtuin 1beta-GalactosidaseGlucoseNF-kappa BPhosphatesSirtuin 1High glucoseHigh phosphateSenescenceSIRT1Vascular calcification

Identifiers

PMID35396645
OpenAlexW4223508055

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.