Evidence map›Paper›PMID 37157174›Full record

ArticleThe Korean journal of internal medicine2023

CTLA4-Ig protects tacrolimus-induced oxidative stress via inhibiting the AKT/FOXO3 signaling pathway in rats.

Long Jin, Nan Shen, Xinyu Wen, Weidong Wang, Sun Woo Lim, Chul Woo Yang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Korean journal of internal medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.8field-weighted citation impact, top 32% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. 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 3 institutions in 3 countries.

Long JinDepartment of Nephrology, The First Affiliated Hospital of Dalian Medical University, Dalian, China.
Nan ShenDepartment of Nephrology, The First Affiliated Hospital of Dalian Medical University, Dalian, China.
Xinyu WenDepartment of Nephrology, The First Affiliated Hospital of Dalian Medical University, Dalian, China.
Weidong WangDepartment of Nephrology, The First Affiliated Hospital of Dalian Medical University, Dalian, China.
Sun Woo LimTransplant Research Center, College of Medicine, The Catholic University of Korea, Seoul, Korea.
Chul Woo YangTransplant Research Center, College of Medicine, The Catholic University of Korea, Seoul, Korea.
Dalian Medical University · CNKorea Center for Disease Control and Prevention · KRThe Catholic University of Korea Seoul St. Mary's Hospital · KR

Funding

Ministry of Science and ICTNational Natural Science Foundation of China 81900681National Research Foundation of Korea 2020R1A2C201271113
6 · The paper itself

Abstract

BACKGROUND/

aimsAlthough the conversion from tacrolimus (TAC) to cytotoxic T-lymphocyte-associated antigen 4-immunoglobulin (CTLA4-Ig) is effective in reducing TAC-induced nephrotoxicity, it remains unclear whether CTLA4-Ig has a direct effect on TAC-induced renal injury. In this study, we evaluated the effects of CTLA4-Ig on TAC-induced renal injury in terms of oxidative stress.

methodsIn vitro study was performed to assess the effect of CTLA4-Ig on TAC-induced cell death, reactive oxygen species (ROS), apoptosis, and the protein kinase B (AKT)/forkhead transcription factor (FOXO) 3 pathway in human kidney 2 cells. In the in vivo study, the effect of CTLA4-Ig on TAC-induced renal injury was evaluated using renal function, histopathology, markers of oxidative stress (8-hydroxy-2'-deoxyguanosine) and metabolites (4-hydroxy-2-hexenal, catalase, glutathione S-transferase, and glutathione reductase), and activation of the AKT/FOXO3 pathway with insulin-like growth factor 1 (IGF-1).

resultsCTLA4-Ig significantly decreased cell death, ROS, and apoptosis caused by TAC. TAC treatment increased apoptotic cell death and apoptosis-related proteins (increased Bcl-2-associated X protein and caspase-3 and decreased Bcl-2), but it was reversed by CTLA4-Ig treatment. The activation of p-AKT and p-FOXO3 by TAC decreased with CTLA4-Ig treatment. TAC-induced renal dysfunction and oxidative marker levels were significantly improved by CTLA4-Ig in vivo. Concomitant IGF-1 treatment abolished the effects of CTLA4-Ig.

conclusionCTLA4-Ig has a direct protective effect on TAC-induced renal injury via the inhibition of AKT/FOXO3 pathway.

Indexed as

Renal InsufficiencyTacrolimusAbataceptAnimalsApoptosisApoptosis Regulatory ProteinsCTLA-4 AntigenForkhead Box Protein O3HumansInsulin-Like Growth Factor IOxidative StressProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleyReactive Oxygen SpeciesSignal TransductionAbataceptApoptosis Regulatory ProteinsCTLA-4 AntigenCTLA4 protein, humanForkhead Box Protein O3FOXO3 protein, humanInsulin-Like Growth Factor IProto-Oncogene Proteins c-aktReactive Oxygen SpeciesTacrolimusAKT/FOXO3 signaling pathwayCTLA4-IgRenal injuryTacrolimus

Identifiers

PMID37157174
PMCPMC10175874
OpenAlexW4367316478

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.