Evidence map›Paper›PMID 32627655›Full record

ArticleCell cycle (Georgetown, Tex.)2020

LncRNA SNHG17 knockdown promotes Parkin-dependent mitophagy and reduces apoptosis of podocytes through Mst1.

Feng Guo, Weimin Wang, Yi Song, Lina Wu, Jiao Wang, Yanyan Zhao, Xiaojun Ma, Hongfei Ji, Yanling Liu, Zhizhen Li and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

26 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Autophagy and Mitophagy in Diabetic Kidney Disease-A Literature Review.International journal of molecular sciences · 2025
    Review
  10. Review
  11. Translational cancer research · 2024
    Article
  12. Review
  13. Article
  14. Mechanisms and implications of podocyte autophagy in chronic kidney disease.American journal of physiology. Renal physiology · 2024
    Review
  15. Article
  16. Article
  17. Review
  18. Long Non-Coding RNAs as "MYC Facilitators".Pathophysiology : the official journal of the International Society for Pathophysiology · 2023
    Review
  19. Review
  20. Article
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

11 authors at 1 institution in 1 country.

Feng GuoDivision of Endocrinology, Department of Internal Medicine, The First Affiliated Hospital of Zhengzhou University , Zhengzhou, China.
Weimin WangDivision of Hematology, Department of Internal Medicine, The First Affiliated Hospital of Zhengzhou University , Zhengzhou, China.
Yi SongDivision of Endocrinology, Department of Internal Medicine, The First Affiliated Hospital of Zhengzhou University , Zhengzhou, China.
Lina WuDivision of Endocrinology, Department of Internal Medicine, The First Affiliated Hospital of Zhengzhou University , Zhengzhou, China.
Jiao WangDivision of Endocrinology, Department of Internal Medicine, The First Affiliated Hospital of Zhengzhou University , Zhengzhou, China.
Yanyan ZhaoDivision of Endocrinology, Department of Internal Medicine, The First Affiliated Hospital of Zhengzhou University , Zhengzhou, China.
Xiaojun MaDivision of Endocrinology, Department of Internal Medicine, The First Affiliated Hospital of Zhengzhou University , Zhengzhou, China.
Hongfei JiDivision of Endocrinology, Department of Internal Medicine, The First Affiliated Hospital of Zhengzhou University , Zhengzhou, China.
Yanling LiuDivision of Endocrinology, Department of Internal Medicine, The First Affiliated Hospital of Zhengzhou University , Zhengzhou, China.
Zhizhen LiDivision of Endocrinology, Department of Internal Medicine, The First Affiliated Hospital of Zhengzhou University , Zhengzhou, China.
Guijun QinDivision of Endocrinology, Department of Internal Medicine, The First Affiliated Hospital of Zhengzhou University , Zhengzhou, China.
First Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

LncRNAs play important roles in the regulation of podocyte apoptosis in diabetic nephropathy (DN). However, the role of lncRNA SNHG17 in controlling mitophagy-induced apoptosis of podocytes in DN is unknown. This study aims to elucidate the underlying mechanism of lncRNA SNHG17 in the regulation of mitophagy-induced apoptosis of podocytes in DN. LncRNA SNHG17 and Mammalian Sterile 20-like kinase 1 (Mst1) expression were upregulated in glomeruli and podocytes of DM mice and high glucose-treated podocytes, whereas Parkin expression was downregulated. LncRNA SNHG17 overexpression suppressed mitophagy and induced apoptosis of podocytes while silencing lncRNA SNHG17 promoted mitophagy and reduced the apoptosis of podocytes. In addition, lncRNA SNHG17 interacted with Mst1 and regulated the degradation of Mst1. We further found lncRNA SNHG17 regulated Parkin expression through Mst1. Mechanistically, lncRNA SNHG17 regulated Parkin-dependent mitophagy and apoptosis of podocytes through regulating Mst1. Finally, silencing lncRNA SNHG17 promoted mitophagy and relieved DN

Indexed as

Gene Knockdown TechniquesAnimalsApoptosisDiabetic NephropathiesHippo KinasesMaleMice, Inbred C57BLMitophagyPodocytesProtein Serine-Threonine KinasesProteolysisRNA, Long NoncodingUbiquitin-Protein LigasesHippo Kinasesparkin proteinProtein Serine-Threonine KinasesRNA, Long NoncodingStk4 protein, mouseUbiquitin-Protein Ligasesapoptosisdiabetic nephropathylncRNA SNHG17mitophagyMst1Parkin

Identifiers

PMID32627655
PMCPMC7469517
OpenAlexW3038423521

What Socratic holds

Textmetadata
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 Socratic graph.