Evidence map›Paper›PMID 35277475›Full record

ArticleCell death & disease2022

Oxidative phosphorylation promotes vascular calcification in chronic kidney disease.

Jia Shi, Yi Yang, Ya-Nan Wang, Qing Li, Xue Xing, An-Ying Cheng, Xiao-Na Zhan, Jie Li, Gang Xu, Fan He

Abstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

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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

10 authors.

Jia ShiDepartment of Nephrology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095, Wuhan, Jiefang Ave, China.
Yi YangDepartment of Nephrology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095, Wuhan, Jiefang Ave, China.
Ya-Nan WangDepartment of Nephrology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095, Wuhan, Jiefang Ave, China.
Qing LiDepartment of Nephrology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095, Wuhan, Jiefang Ave, China.
Xue XingDepartment of Nephrology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095, Wuhan, Jiefang Ave, China.
An-Ying ChengDepartment of Nephrology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095, Wuhan, Jiefang Ave, China.
Xiao-Na ZhanDepartment of Nephrology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095, Wuhan, Jiefang Ave, China.
Jie LiDepartment of Nephrology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095, Wuhan, Jiefang Ave, China.
Gang XuDepartment of Nephrology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095, Wuhan, Jiefang Ave, China. xugang@tjh.tjmu.edu.cn.ORCID 0000-0001-6862-0546
Fan HeDepartment of Nephrology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095, Wuhan, Jiefang Ave, China. fhe@tjh.tjmu.edu.cn.ORCID 0000-0002-2487-5827

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolism has been reported to associate with the progression of vascular diseases. However, how vascular calcification in chronic kidney disease (CKD) is regulated by metabolic status remains poorly understood. Using a model of 5/6 nephrectomy, we demonstrated that the aortic tissues of CKD mice had a preference for using oxidative phosphorylation (OXPHOS). Both high phosphate and human uremic serum-stimulated vascular smooth muscle cells (VSMCs) had enhanced mitochondrial respiration capacity, while the glycolysis level was not significantly different. Besides, 2-deoxy-d-glucose (2-DG) exacerbated vascular calcification by upregulating OXPHOS. The activity of cytochrome c oxidase (COX) was higher in the aortic tissue of CKD mice than those of sham-operated mice. Moreover, the expression levels of COX15 were higher in CKD patients with aortic arch calcification (AAC) than those without AAC, and the AAC scores were correlated with the expression level of COX15. Suppressing COX sufficiently attenuated vascular calcification. Our findings verify the relationship between OXPHOS and calcification, and may provide potential therapeutic approaches for vascular calcification in CKD.

Indexed as

Renal Insufficiency, ChronicVascular CalcificationAnimalsElectron Transport Complex IVFemaleHumansMaleMiceMyocytes, Smooth MuscleOxidative PhosphorylationPhosphatesCOX15 protein, humanElectron Transport Complex IVPhosphates

Identifiers

PMID35277475
PMCPMC8917188

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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.