Evidence map›Paper›PMID 34533106›Full record

ArticleBioengineered2021

Nucleoporin 160 (NUP160) inhibition alleviates diabetic nephropathy by activating autophagy.

Jiayong Xie, Ying Yuan, Gang Yao, Zhi Chen, Wenjuan Yu, Qiang Zhu

Open access · goldAbstract read
In one paragraph

Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Advances in the understanding of nuclear pore complexes in human diseases.Journal of cancer research and clinical oncology · 2024
    Review
  7. Targeting super-enhancer activity for colorectal cancer therapy.American journal of translational research · 2024
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Helicobacter pyloriBioengineered · 2022
    Article
  13. 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

6 authors at 2 institutions in 1 country.

Jiayong XieDepartment of Nephrology, Xinghua People's Hospital, Taizhou Jiangsu, China.
Ying YuanDepartment of Nephrology, Xinghua People's Hospital, Taizhou Jiangsu, China.
Gang YaoDepartment of Nephrology, Second Affiliated Hospital of Nanjing Medical University, Nanjing Jiangsu, China.
Zhi ChenDepartment of Laboratory, Xinghua People's Hospital, Taizhou Jiangsu, China.
Wenjuan YuDepartment of Nephrology, Second Affiliated Hospital of Nanjing Medical University, Nanjing Jiangsu, China.
Qiang ZhuDepartment of Nephrology, Xinghua People's Hospital, Taizhou Jiangsu, China.ORCID 0000-0003-1535-0364
Xintai People's Hospital · CNSecond Affiliated Hospital of Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic nephropathy (DN) is the leading cause of end-stage renal disease worldwide. Autophagy was reported to be related to the pathogenesis of DN. This research investigated the function of the Nucleoporin 160 (Nup160) gene in regulating autophagy in DN. A mouse model of DN was established through an intraperitoneal injection of streptozotocin (STZ). Normal rat kidney tubular epithelial cells (NRK-52E) were treated with high glucose to induce DN in vitro. Real-time quantitative polymerase chain reaction (RT-qPCR), western blot, immunofluorescence assays were conducted to measure the expression of NUP160, autophagy-associated proteins, and inflammatory cytokines in vitro and in vivo. Pathological changes of kidney and liver tissues were analyzed using hematoxylin and eosin (H&E), Masson and periodic acid-silver (PAS) staining. The body weight, blood glucose, renal and lipid profiles of DN mice were examined. In this study, DN mice showed serious pathological injury. NUP160 expression was upregulated, autophagy was inhibited, and inflammatory response was increased in DN mice. Depletion of NUP160 restored autophagy and inhibited inflammation and fibrosis in high glucose (HG)-treated NRK-52E cells and STZ-induced DN mice by downregulating the expression of p62 and Collagen IV (Col-Ⅳ), increasing the ratio of LC3II/LC3I, and inactivating nuclear factor (NF)-κB signaling. Moreover, NUP160 knockdown could ameliorate pathological damage and glucose tolerance in DN mice. Overall, this study is the first to demonstrate the key role of NUP160 silencing in promoting autophagy against diabetic injury in DN.

Indexed as

Nuclear Pore Complex ProteinsAnimalsAutophagyCells, CulturedDiabetes Mellitus, ExperimentalDiabetic NephropathiesFibrosisInflammationMaleMiceMice, Inbred C57BLRatsSignal TransductionNuclear Pore Complex Proteinsautophagydiabetic nephropathyinflammatory responseNUP160

Identifiers

PMID34533106
PMCPMC8806760
OpenAlexW3200856010

What OpenQuestion holds

Textmetadata
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.