Evidence map›Paper›PMID 33159018›Full record

ArticleAging2020

Cyclooxygenase-2/sclerostin mediates TGF-β1-induced calcification in vascular smooth muscle cells and rats undergoing renal failure.

Fang He, Ling Li, Pei-Pei Li, Yan Deng, Yuan-Yuan Yang, Yi-Xuan Deng, Hong-Hong Luo, Xin-Tong Yao, Yu-Xi Su, Hua Gan and 1 more

Open access · greenAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.0field-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

12 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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  10. Review
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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

11 authors at 3 institutions in 1 country.

Fang HeDepartment of Pharmacology, School of Pharmacy, Chongqing Medical University, Chongqing 400016, China.
Ling LiDepartment of Pharmacology, School of Pharmacy, Chongqing Medical University, Chongqing 400016, China.
Pei-Pei LiDepartment of Pharmacology, School of Pharmacy, Chongqing Medical University, Chongqing 400016, China.
Yan DengDepartment of Pharmacology, School of Pharmacy, Chongqing Medical University, Chongqing 400016, China.
Yuan-Yuan YangDepartment of Pharmacology, School of Pharmacy, Chongqing Medical University, Chongqing 400016, China.
Yi-Xuan DengDepartment of Pharmacology, School of Pharmacy, Chongqing Medical University, Chongqing 400016, China.
Hong-Hong LuoDepartment of Pharmacology, School of Pharmacy, Chongqing Medical University, Chongqing 400016, China.
Xin-Tong YaoDepartment of Pharmacology, School of Pharmacy, Chongqing Medical University, Chongqing 400016, China.
Yu-Xi SuDepartment of Orthopedic, Children Hospital of Chongqing Medical University, Chongqing 400014, China.
Hua GanDepartment of Nephrology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Bai-Cheng HeDepartment of Pharmacology, School of Pharmacy, Chongqing Medical University, Chongqing 400016, China.
Chongqing Medical University · CNChildren's Hospital of Chongqing Medical University · CNFirst Affiliated Hospital of Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this study, we studied the effect and possible mechanism of TGF-β1 on vascular calcification. We found that the serum levels of TGF-β1 and cycloxygenase-2 (COX-2) were significantly increased in patients with chronic kidney disease. Phosphate up regulated TGF-β1 in vascular smooth muscle cells (VSMCs). TGF-β1 decreased the markers of VSMCs, but increased osteogenic markers and calcification in aortic segments. The phosphate-induced osteogenic markers were reduced by the TGFβR I inhibitor (LY364947), which also attenuated the potential of phosphate to reduce VSMC markers in VSMCs. Both phosphate and TGF-β1 increased the protein level of β-catenin, which was partially mitigated by LY364947. TGF-β1 decreased sclerostin, and exogenous sclerostin decreased the mineralization induced by TGF-β1. LY364947 reduced the phosphate and TGF-β1 induced COX-2. Meanwhile, the effects of TGF-β1 on osteogenic markers, β-catenin, and sclerostin, were partially reversed by the COX-2 inhibitor. Mechanistically, we found that p-Smad2/3 and p-CREB were both enriched at the promoter regions of sclerostin and β-catenin. TGF-β1 and COX-2 were significantly elevated in serum and aorta of rats undergoing renal failure. Therapeutic administration of meloxicam effectively ameliorated the renal lesion. Our results suggested that COX-2 may mediate the effect of TGF-β1 on vascular calcification through down-regulating sclerostin in VMSCs.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsBiomarkersCalcinosisCells, CulturedCyclooxygenase 2HEK293 CellsHumansMaleMuscle, Smooth, VascularRats, Sprague-DawleyRenal InsufficiencyTransforming Growth Factor beta1Adaptor Proteins, Signal TransducingBiomarkersCyclooxygenase 2SOST protein, humanTransforming Growth Factor beta1chronic kidney diseaseCOX-2sclerostinTGF-β1vascular calcification

Identifiers

PMID33159018
PMCPMC7695383
OpenAlexW3097091935

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.