Evidence map›Paper›PMID 35922749›Full record

ArticleMolecular medicine (Cambridge, Mass.)2022

Oxalate-induced apoptosis through ERS-ROS-NF-κB signalling pathway in renal tubular epithelial cell.

Shaoxiong Ming, Jia Tian, Ke Ma, Chengbin Pei, Ling Li, Zeyu Wang, Ziyu Fang, Min Liu, Hao Dong, Weijian Li and 3 more

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 1 pooled it
14.7field-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

75 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.

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  19. A novel role ofMicrobiology spectrum · 2026
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15 more citing papers are in PubMed but not listed here.

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

13 authors at 3 institutions in 1 country.

Shaoxiong Ming *Department of Urology, Changhai Hospital of Shanghai, No. 168, Changhai Road, Yangpu District, Shanghai, 200433, China.
Jia Tian *Department of Human Sperm Bank of Ningxia, General Hospital of Ningxia Medical University, Ningxia Medical University, No. 804 Shengli South Street, Xingqing District, Yinchuan, 750001, Ningxia Hui Autonomous Region, China.
Ke Ma *Department of Urology, Changhai Hospital of Shanghai, No. 168, Changhai Road, Yangpu District, Shanghai, 200433, China.
Chengbin PeiDepartment of Human Sperm Bank of Ningxia, General Hospital of Ningxia Medical University, Ningxia Medical University, No. 804 Shengli South Street, Xingqing District, Yinchuan, 750001, Ningxia Hui Autonomous Region, China.
Ling LiDepartment of Urology, Changhai Hospital of Shanghai, No. 168, Changhai Road, Yangpu District, Shanghai, 200433, China.
Zeyu WangDepartment of Urology, Changhai Hospital of Shanghai, No. 168, Changhai Road, Yangpu District, Shanghai, 200433, China.
Ziyu FangDepartment of Urology, Changhai Hospital of Shanghai, No. 168, Changhai Road, Yangpu District, Shanghai, 200433, China.
Min LiuDepartment of Urology, Changhai Hospital of Shanghai, No. 168, Changhai Road, Yangpu District, Shanghai, 200433, China.
Hao DongDepartment of Urology, Changhai Hospital of Shanghai, No. 168, Changhai Road, Yangpu District, Shanghai, 200433, China.
Weijian LiDepartment of Urology, Sixth Affiliated Hospital of Guangzhou Medical University (Qingyuan People's Hospital), B24, Yinquan Road, XinchengDistrict, Qingyuan, 511518, Guangdong Province, China.
Jianwen ZengDepartment of Urology, Sixth Affiliated Hospital of Guangzhou Medical University (Qingyuan People's Hospital), B24, Yinquan Road, XinchengDistrict, Qingyuan, 511518, Guangdong Province, China.
Yonghan Peng *Department of Urology, Changhai Hospital of Shanghai, No. 168, Changhai Road, Yangpu District, Shanghai, 200433, China. yonghanyhtl@163.com.
Xiaofeng Gao *Department of Urology, Changhai Hospital of Shanghai, No. 168, Changhai Road, Yangpu District, Shanghai, 200433, China. gxfdoc@sina.com.ORCID 0000-0002-6489-5750
Second Military Medical University · CNGuangzhou Medical University · CNNingxia Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundKidney stones are composed of approximately 70-80% calcium oxalate. However, the exact mechanism of formation of calcium oxalate kidney stones remains unclear. In this study, we investigated the roles of endoplasmic reticulum stress (ERS), reactive oxygen species (ROS), and the NF-κB signalling pathway in the pathogenesis of oxalate-induced renal tubular epithelial cell injury and its possible molecular mechanisms.

methodsWe established a model to evaluate the formation of kidney stones by intraperitoneal injection of glyoxylic acid solution into mice and assessed cell morphology, apoptosis, and the expression levels of ERS, ROS, and NF-κB signalling pathway-related proteins in mouse renal tissues. Next, we treated HK-2 cells with potassium oxalate to construct a renal tubular epithelial cell injury model. We detected the changes in autophagy, apoptosis, and mitochondrial membrane potential and investigated the ultrastructure of the cells by transmission electron microscopy. Western blotting revealed the expression levels of apoptosis and autophagy proteins; mitochondrial structural and functional proteins; and ERS, ROS, and NF-κB (p65) proteins. Lastly, we studied the downregulation of NF-κB activity in HK-2 cells by lentivirus interference and confirmed the interaction between the NF-κB signalling and ERS/ROS pathways.

resultsWe observed swelling of renal tissues, increased apoptosis of renal tubular epithelial cells, and activation of the ERS, ROS, and NF-κB signalling pathways in the oxalate group. We found that oxalate induced autophagy, apoptosis, and mitochondrial damage in HK-2 cells and activated the ERS/ROS/NF-κB pathways. Interestingly, when the NF-κB signalling pathway was inhibited, the ERS/ROS pathway was also inhibited.

conclusionOxalate induces HK-2 cell injury through the interaction between the NF-κB signalling and ERS/ROS pathways.

Indexed as

Endoplasmic Reticulum StressKidney CalculiAnimalsApoptosisCalcium OxalateEpithelial CellsMiceNF-kappa BOxalatesReactive Oxygen SpeciesCalcium OxalateNF-kappa BOxalatesReactive Oxygen SpeciesEndoplasmic reticulum stress (ERS)Kidney stonesNF-κB signalling pathwayOxalateReactive oxygen species (ROS)

Identifiers

PMID35922749
PMCPMC9347104
OpenAlexW4289544400

What OpenQuestion holds

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LicenceCC BY
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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.