Evidence map›Paper›PMID 36449224›Full record

ArticleInternational urology and nephrology2023

Tripartite motif containing 23 functions as a critical regulator in macrophages to control the pathological feature of diabetic nephropathy.

Wei Quan, Lin Wang

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Article in International urology and nephrology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.1field-weighted citation impact, top 51% of its field
1 · What the graph read from it

What it found

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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

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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

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0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Wei Quan *Department of Endocrinology, Daqing Oilfield General Hospital, No. 9, Zhongkang Street, Sartu District, Daqing, 163000, Heilongjiang, China.
Lin Wang *Department of Endocrinology, Daqing Oilfield General Hospital, No. 9, Zhongkang Street, Sartu District, Daqing, 163000, Heilongjiang, China. wanglin63665662022@163.com.
Daqing Oilfield General Hospital · CN

Funding

Health Scientific project of Heilongjiang Province 2020-372
6 · The paper itself

Abstract

backgroundDiabetic nephropathy (DN) is a kidney disease resulting from diabetes. Macrophages and macrophage-mediated inflammation contributed to the development of DN. Tripartite motif containing 23 (TRIM23) is E3 ligase and has been involved in inflammation. Until now, the precise roles of TRIM23 in DN are not described yet. Therefore, we evaluated the functions of TRIM23 in DN.

methodsWe generated mice with TRIM23 deficiency in macrophages. We also established diabetic mice model. The expression of TRIM23 was measured in diabetic animals. The DN symptoms were compared between diabetic wild-type (WT) mice and TRIM23 conditional knock out mice. The cytokine expression, ubiquitination of TAB2, and interactions between TAB2 and IKK were compared in oxidized low-density lipoprotein (oxLDL) or lipopolysaccharides (LPS)-treated WT and TRIM23-deficient macrophages.

resultsUpregulation of TRIM23 was observed in diabetic mice and LPS or oxLDL-treated macrophages. Diabetic mice with TRIM23 deficiency in macrophages had attenuated DN symptoms. TRIM23-deficient macrophages had decreased pro-inflammatory cytokines production after oxLDL or LPS stimulation. TRIM23 was predicted to interact with TAB2. The ubiquitination of TAB2 was abolished in oxLDL-treated TRIM23-deficient macrophages, which correlated with decreased activation of IKK.

conclusionTRIM23 regulates inflammation in macrophages and plays important role in DN.

Indexed as

Diabetes Mellitus, ExperimentalDiabetic NephropathiesAnimalsInflammationLipopolysaccharidesMacrophagesMiceMice, KnockoutLipopolysaccharidesDiabetic nephropathyInflammationMacrophagesTRIM23

Identifiers

PMID36449224
OpenAlexW4310465409

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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.