Evidence map›Paper›PMID 33978765›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2021

Silencing circANKRD36 inhibits streptozotocin-induced insulin resistance and inflammation in diabetic rats by targeting miR-145 via XBP1.

Jinger Lu, Linrong Pang, Bo Zhang, Zhigang Gong, Chunhui Song

RetractedAbstract readRetracted Publication
PubMed Publisher
In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 24% 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, 21 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Jinger LuDepartment of Endocrinology, The Affiliated People's Hospital of Ningbo University, Ningbo, 315040, Zhejiang, China.
Linrong PangDepartment of Chemoradiotherapy Centre, The Affiliated People's Hospital of Ningbo University, Ningbo, 315040, Zhejiang, China.
Bo ZhangDepartment of Infectious Disease, The Affiliated People's Hospital of Ningbo University, Ningbo, 315040, Zhejiang, China.
Zhigang GongCollege of Physical Education, Jiangxi Normal University, Nanchang, 330022, Jiangxi, China.
Chunhui SongCollege of Life Sciences, Jiangxi Normal University, No. 99 Ziyang Avenue, Nanchang, 330022, Jiangxi, China. songch1919@163.com.ORCID http://orcid.org/0000-0001-9499-3557
Ningbo University · CNJiangxi Normal University · CN

Funding

Innovative Research Group Project of the National Natural Science Foundation of China (CN) 81560766Provincial Medical and Health Science and Technology Plan 2019KY019
6 · The paper itself

Abstract

backgroundDiabetes mellitus (DM) is defined as a group of metabolic diseases characterized by hyperglycemia, which results from a deficiency in insulin secretion and/or insulin action. In diabetic patients, type 2 diabetes mellitus (T2DM) is in the majority. We explored the effects of circANKRD36 on streptozotocin (STZ)-induced insulin resistance and inflammation in diabetic rats with the aim of uncovering the underlying mechanism.

methodsSTZ was used to induce the in vivo T2DM rat model. After circANKRD36 interference, blood glucose, insulin and adiponectin were respectively detected. Hematoxylin and eosin (H&E), enzyme-linked immunosorbent assay (ELISA) and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay (TUNEL) were conducted to examine inflammation and apoptosis in T2DM rats, and western blot was used for detecting apoptosis-related proteins. The binding relationships among circANKRD36, miR-145 and XBP1 were examined by luciferase reporter assay.

resultsResults showed that circANKRD36 was expressed at a high level in T2DM rats, while silencing circANKRD36 led to decreased blood glucose and insulin, accompanied by increased adiponectin level, and ameliorating insulin resistance. Silencing circANKRD36 alleviated the inflammation and suppressed cell apoptosis in the pancreatic tissues of T2DM rats, which was abated by miR-145 inhibitor. The binding of miR-145 to XBP1 was then confirmed. Additionally, miR-145 inhibitor increased the level of XBP1 in T2DM rats, which was decreased in the presence of circANKRD36 silencing.

conclusionThis study is the first to prove that silencing circANKRD36 inhibits STZ-induced insulin resistance and inflammation in diabetic rats by targeting miR- 145 via XBP1. The results warrant the importance of circRNAs as drug target and thereby pave way for the development of newer therapeutic measures for T2DM.

Indexed as

MicroRNAsRNA, CircularAnimalsCytokinesDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2InflammationInsulin ResistanceMalePancreasRatsRats, Sprague-DawleyUp-RegulationX-Box Binding Protein 1CytokinesMicroRNAsMIRN145 microRNA, ratRNA, CircularX-Box Binding Protein 1Xbp1 protein, ratCircANKRD36InflammationInsulin resistanceMiR-145Type 2 diabetes mellitus

Identifiers

PMID33978765
OpenAlexW3161579622

What OpenQuestion 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 OpenQuestion graph.