Evidence map›Paper›PMID 38464366›Full record

ArticleWorld journal of diabetes2024

Long noncoding RNA protein-disulfide isomerase-associated 3 regulated high glucose-induced podocyte apoptosis in diabetic nephropathy through targeting miR-139-3p.

Yin-Xi He, Ting Wang, Wen-Xian Li, Yan-Xia Chen

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Article in World journal of diabetes, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

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3citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Article
  2. Characterizing Circulating microRNA Signatures of Type 2 Diabetes Subtypes.International journal of molecular sciences · 2025
    Article
  3. Review
4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Yin-Xi HeDepartment of Orthopaedic Trauma, The Third Hospital of Shijiazhuang, Shijiazhuang 050000, Hebei Province, China.
Ting WangDepartment of Endocrinology, The Second Hospital of Hebei Medical University, Shijiazhuang 050000, Hebei Province, China.
Wen-Xian LiDepartment of Endocrinology, The First Hospital of Zhangjiakou, Zhangjiakou 075000, Hebei Province, China.
Yan-Xia ChenDepartment of Endocrinology, The Second Hospital of Hebei Medical University, Shijiazhuang 050000, Hebei Province, China. chenyx@hebmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPodocyte apoptosis plays a vital role in proteinuria pathogenesis in diabetic nephropathy (DN). The regulatory relationship between long noncoding RNAs (lncRNAs) and podocyte apoptosis has recently become another research hot spot in the DN field.

aimTo investigate whether lncRNA protein-disulfide isomerase-associated 3 (Pdia3) could regulate podocyte apoptosis through miR-139-3p and revealed the underlying mechanism.

methodsUsing normal glucose or high glucose (HG)-cultured podocytes, the cellular functions and exact mechanisms underlying the regulatory effects of lncRNA Pdia3 on podocyte apoptosis and endoplasmic reticulum stress (ERS) were explored. LncRNA Pdia3 and miR-139-3p expression were measured through quantitative real-time polymerase chain reaction. Relative cell viability was detected through the cell counting kit-8 colorimetric assay. The podocyte apoptosis rate in each group was measured through flow cytometry. The interaction between lncRNA Pdia3 and miR-139-3p was examined through the dual luciferase reporter assay. Finally, western blotting was performed to detect the effect of lncRNA Pdia3 on podocyte apoptosis and ERS

resultsThe expression of lncRNA Pdia3 was significantly downregulated in HG-cultured podocytes. Next, lncRNA Pdia3 was involved in HG-induced podocyte apoptosis. Furthermore, the dual luciferase reporter assay confirmed the direct interaction between lncRNA Pdia3 and miR-139-3p. LncRNA Pdia3 overexpression attenuated podocyte apoptosis and ERS through miR-139-3p in HG-cultured podocytes.

conclusionTaken together, this study demonstrated that lncRNA Pdia3 overexpression could attenuate HG-induced podocyte apoptosis and ERS by acting as a competing endogenous RNA of miR-139-3p, which might provide a potential therapeutic target for DN.

Indexed as

Competing endogenous RNADiabetic nephropathyEndoplasmic reticulum stressLong noncoding RNAsPodocyte apoptosis

Identifiers

PMID38464366
PMCPMC10921158

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