Evidence map›Paper›PMID 31017263›Full record

ArticleInternational journal of molecular medicine2019

Role of the thioredoxin interacting protein in diabetic nephropathy and the mechanism of regulating NOD‑like receptor protein 3 inflammatory corpuscle.

Chunmei Gu, Shumei Liu, Hongyue Wang, Haichuan Dou

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

28 citing papers in PubMed, 45 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Chunmei GuDepartment of Nephrology, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.
Shumei LiuDepartment of Endocrinology, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.
Hongyue WangDepartment of Nephrology, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.
Haichuan DouDepartment of Nephrology, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.
First Hospital of Jilin University · CNJilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory response serves an important role in diabetic nephropathy (DN); however, the mechanism of inflammatory response results in renal damage is not yet clear. The aim of the present study was to investigate the role of the thioredoxin interacting protein (TXNIP)/NOD‑like receptor protein 3 (NLRP3) axis‑mediated activation of NLRP3 inflammasome in DN. A diabetic rat model was induced by streptozotocin injection. Hematoxylin and eosin (H&E) staining and streptavidin‑peroxidase staining were then used to examine the kidney tissue morphology, and TXNIP and NLRP3 protein expression levels, respectively. Furthermore, RNA interference technology was applied to silence the TXNIP gene. TXNIP and NLRP3 inflammasome activation‑associated proteins and mRNAs were detected by western blot analysis and RT‑qPCR, respectively. Enzyme‑linked immunosorbent assay was also used to examine interleukin (IL)‑1 and IL‑18 expression, while flow cytometry was performed to detect reactive oxygen species production. The data revealed that TXNIP and NLRP3 were overexpressed in kidney tissue of DN rats, and the level of antioxidant genes was downregulated. It was also observed that glucose promoted TXNIP expression and activation of NLRP3 inflammasome in a time‑dependent and dose‑dependent manner, therefore promoting inflammatory responses. Silencing of TXNIP gene resulted in the downregulation of NLRP3 inflammasome activation, and inhibited the expression levels of IL‑1 and IL‑18 in a high‑glucose environment. Furthermore, low expression of TXNIP promoted the levels of antioxidant genes and reduced the ROS levels. Taken together, the high‑glucose environment was able to upregulated the level of inflammatory factors by promoting the expression of TXNIP and the activation of NLRP3 inflammasome, consequently participating in DN.

Indexed as

AnimalsCarrier ProteinsCell Cycle ProteinsCell LineDiabetes Mellitus, ExperimentalDiabetic NephropathiesGlucoseHumansInflammasomesInflammationMaleNLR Family, Pyrin Domain-Containing 3 ProteinOxidative StressRats, Sprague-DawleyCarrier ProteinsCell Cycle ProteinsGlucoseInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, ratTXNIP protein, rat

Identifiers

PMID31017263
PMCPMC6488169
OpenAlexW2936782252

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.