Evidence map›Paper›PMID 34608568›Full record

ArticleIn vitro cellular & developmental biology. Animal2021

miR-23a-3p regulates the inflammatory response and fibrosis in diabetic kidney disease by targeting early growth response 1.

Shuyue Sheng, Meina Zou, Yanlin Yang, Meiping Guan, Shijing Ren, Xiangyu Wang, Ling Wang, Yaoming Xue

Open access · hybridAbstract read
In one paragraph

Article in In vitro cellular & developmental biology. Animal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 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

8 authors at 1 institution in 1 country.

Shuyue Sheng *Department of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, No. 1838 Guangzhou North Avenue, Guangzhou, 510515, Guangdong, China.
Meina Zou *Department of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, No. 1838 Guangzhou North Avenue, Guangzhou, 510515, Guangdong, China.
Yanlin YangDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, No. 1838 Guangzhou North Avenue, Guangzhou, 510515, Guangdong, China.
Meiping GuanDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, No. 1838 Guangzhou North Avenue, Guangzhou, 510515, Guangdong, China.
Shijing RenDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, No. 1838 Guangzhou North Avenue, Guangzhou, 510515, Guangdong, China.
Xiangyu WangDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, No. 1838 Guangzhou North Avenue, Guangzhou, 510515, Guangdong, China.
Ling WangDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, No. 1838 Guangzhou North Avenue, Guangzhou, 510515, Guangdong, China.
Yaoming XueDepartment of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, No. 1838 Guangzhou North Avenue, Guangzhou, 510515, Guangdong, China. xueyaoming999@126.com.ORCID http://orcid.org/0000-0003-1356-4780
Nanfang Hospital · CN

Funding

National Natural Science Foundation of China 81870570National Natural Science Foundation of China 82070848
6 · The paper itself

Abstract

Diabetic kidney disease (DKD) has become the most common cause of chronic kidney disease. Proteinuria is generally considered one of the clinical indicators of renal damage, and it is also closely related to the progression of DKD. Accumulating evidence indicates that proteinuria induces an upregulation of the expression levels of inflammatory cytokines and fibrosis markers in renal tubular epithelial cells, but the mechanism remains unclear. Previously, we showed that early growth response 1 (Egr1) played a key role in renal tubular injury. However, the upstream mechanism of Egr1 in the development of DKD is poorly understood. In this study, we found that albumin stimulation significantly increased the expression levels of Egr1, interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α), and fibronectin (FN) in HK-2 cells but decreased miR-23a-3p levels. We then identified that miR-23a-3p targeted the 3' untranslated region (UTR) of Egr1 and directly suppressed the expression of Egr1. Moreover, we found that overexpression and inhibition of miR-23a-3p in HK-2 cells attenuated and promoted the expression of IL-6, TNF-α, and FN, respectively. Additionally, Egr1 silencing reversed the inflammation and fibrosis caused by the miR-23a-3p inhibitor. Thus, we conclude that miR-23a-3p attenuates the development of DKD through Egr1, suggesting that targeting miR-23a-3p may be a novel therapeutic approach for DKD.

Indexed as

AnimalsBlotting, WesternCell LineDiabetic NephropathiesEarly Growth Response Protein 1FibronectinsFibrosisHEK293 CellsHumansInflammationInterleukin-6Kidney Tubules, ProximalMaleMiceMice, Inbred C57BLMicroRNAsEarly Growth Response Protein 1EGR1 protein, humanFibronectinsIL6 protein, humanInterleukin-6MicroRNAsMIRN23a microRNA, humanTumor Necrosis Factor-alphaDiabetic kidney diseaseEarly growth response 1Inflammatory responsemiRNARenal fibrosis

Identifiers

PMID34608568
PMCPMC8585819
OpenAlexW3201942760

What OpenQuestion holds

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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.