Evidence map›Paper›PMID 37315165›Full record

ArticleJournal of diabetes investigation2023

LncRNA SNHG1 knockdown inhibits hyperglycemia induced ferroptosis via miR-16-5p/ACSL4 axis to alleviate diabetic nephropathy.

Xiangdong Fang, Jianling Song, Yanxia Chen, Shuying Zhu, Weiping Tu, Ben Ke, Lidong Wu

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
8.9field-weighted citation impact, top 2% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
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  10. METTL3/YTHDF3 mJournal of diabetes investigation · 2025
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  16. Noncoding RNAs and diabetic kidney disease.Journal of diabetes investigation · 2025
    Article
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  18. Article
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  20. [Roles of ferroptosis in the development of diabetic nephropathy].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2024
    Review
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

7 authors at 1 institution in 1 country.

Xiangdong FangDepartment of Nephrology, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China.
Jianling SongDepartment of Nephrology, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China.
Yanxia ChenDepartment of Nephrology, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China.
Shuying ZhuDepartment of Nephrology, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China.
Weiping TuDepartment of Nephrology, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China.
Ben KeDepartment of Nephrology, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China.ORCID https://orcid.org/0000-0002-4813-7108
Lidong WuEmergency Department, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China.
Nanchang University · CN

Funding

National Natural Science Foundation of China 82160143The Engineering Research Center of Kidney Disease in Jiangxi Province 20164BCD40095
6 · The paper itself

Abstract

backgroundHyperglycemia accelerates the development of diabetic nephropathy (DN) by inducing renal tubular injury. Nevertheless, the mechanism has not been elaborated fully. Here, the pathogenesis of DN was investigated to seek novel treatment strategies.

methodsA model of diabetic nephropathy was established in vivo, the levels of blood glucose, urine albumin creatinine ratio (ACR), creatinine, blood urea nitrogen (BUN), malondialdehyde (MDA), glutathione (GSH), and iron were measured. The expression levels were detected by qRT-PCR and Western blotting. H&E, Masson, and PAS staining were used to assess kidney tissue injury. The mitochondria morphology was observed by transmission electron microscopy (TEM). The molecular interaction was analyzed using a dual luciferase reporter assay.

resultsSNHG1 and ACSL4 were increased in kidney tissues of DN mice, but miR-16-5p was decreased. Ferrostatin-1 treatment or SNHG1 knockdown inhibited ferroptosis in high glucose (HG)-treated HK-2 cells and in db/db mice. Subsequently, miR-16-5p was confirmed to be a target for SNHG1, and directly targeted to ACSL4. Overexpression of ACSL4 greatly reversed the protective roles of SNHG1 knockdown in HG-induced ferroptosis of HK-2 cells.

conclusionsSNHG1 knockdown inhibited ferroptosis via the miR-16-5p/ACSL4 axis to alleviate diabetic nephropathy, which provided some new insights for the novel treatment of diabetic nephropathy.

Indexed as

Diabetic NephropathiesFerroptosisHyperglycemiaRNA, Long NoncodingAnimalsCreatinineMiceCreatinineRNA, Long NoncodingDiabetic nephropathyLncRNA SNHG1miR-16-5p

Identifiers

PMID37315165
PMCPMC10445199
OpenAlexW4380682947

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LicenceCC BY-NC-ND
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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.