Evidence map›Paper›PMID 41235950›Full record

ArticleBiotechnology and applied biochemistry2026

5-Methylcytosine Analysis of miRNAs in Minimal Change Disease.

Huiyi Zeng, Dandan Li, Yunyi Li, Chen Yun, Xinzhou Zhang, Wenyu Gong, Mengyun Xiao, Haitao Li, Zhipeng Zeng, Ruqi Tan and 5 more

Abstract read
In one paragraph

Article in Biotechnology and applied biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

15 authors.

Huiyi ZengClinical Medical Research Center, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of Southern University of Science and Technology, Shenzhen, China.
Dandan LiForensic Evidence Laboratory, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of Southern University of Science and Technology, Shenzhen, China.
Yunyi LiDepartment of Nephrology, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong, China.
Chen YunDepartment of Nephrology, Charité-Universitätsmedizin Berlin, Campus Mitte, Berlin, Germany.
Xinzhou ZhangDepartment of Nephrology, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of Southern University of Science and Technology, Shenzhen, China.
Wenyu GongDepartment of Nephrology, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong, China.
Mengyun XiaoDepartment of Nephrology, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong, China.
Haitao LiClinical Medical Research Center, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of Southern University of Science and Technology, Shenzhen, China.
Zhipeng ZengClinical Medical Research Center, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of Southern University of Science and Technology, Shenzhen, China.
Ruqi TanClinical Medical Research Center, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of Southern University of Science and Technology, Shenzhen, China.
Yishen YangDepartment of Nephrology, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong, China.
Shaodong LuanDepartment of Nephrology, Shenzhen Longhua District Central Hospital, Shenzhen, Guangdong, China.
Yong DaiClinical Medical Research Center, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of Southern University of Science and Technology, Shenzhen, China.
Lianghong YinClinical Medical Research Center, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of Southern University of Science and Technology, Shenzhen, China.
Donge TangClinical Medical Research Center, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, The First Affiliated Hospital of Southern University of Science and Technology, Shenzhen, China.ORCID https://orcid.org/0000-0001-7011-196X

Funding

Guangdong Engineering Technology Research CenterGuangdong High tech Research and Development Center ProjectGuangdong Provincial Autoimmune Disease Precision Medicine Engineering Research CenterGuangdong Science and Technology ProjectsGuangzhou Development Zone entrepreneurship leading talent projectGuangzhou entrepreneurship leading teamShenzhen Autoimmune Disease Engineering Research Center
6 · The paper itself

Abstract

Minimal change disease (MCD) is a glomerular disorder, which is the most common cause of nephrotic syndrome in children. Additionally, the prevalence of MCD in adults has been increasing in recent years. During protein synthesis, noncoding RNAs can be regulated through a variety of modifications, which helps preserve biological diversity and complexity. This study aims to investigate the role of m5C-modified miRNAs in MCD, with the goal of identifying promising biomarkers and therapeutic targets for patients with this condition. Our findings revealed a substantial number of differentially modified m5C miRNAs in patients with MCD, predominantly exhibiting downregulation of modification. Notable miRNAs showing differential modification included miR-1282, miR-340-3p, miR-526b-3p, miR-3925-3p, and miR-511-5p. Further bioinformatics analysis demonstrated that the pathogenic mechanism of miR-511-5p in MCD may involve lipid metabolism by decreasing the expression of ectonucleotide pyrophosphatase/phosphodiesterase 4 (ENPP4) and ecto-nucleoside triphosphate diphosphohydrolase (ENTPD1). Both m5C writer and target genes had high-confidence interactions with miR-511-5p. This study confirmed the pathogenic role of m5C-modified miRNAs in MCD. The m5C modification of miRNAs in MCD is primarily downregulated, which is likely due to the downregulated of DNMT1. Finally, we focused on the downregulated m5C-modified miR-511-5p, which contributes to MCD by regulating metabolic pathways and decreasing the expression of ENPP4 and ENTPD1.

Indexed as

MicroRNAsNephrosis, LipoidHumansRNA MethylationMicroRNAslipid metabolismm5C modificationmetabolic pathwayminimal change diseasemiRNA

Identifiers

PMID41235950
PMCPMC13238414

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.