Evidence map›Paper›PMID 31655428›Full record

ArticleRedox biology2020

SIRT3-mediated deacetylation of PRDX3 alleviates mitochondrial oxidative damage and apoptosis induced by intestinal ischemia/reperfusion injury.

Zhanyu Wang, Ruimin Sun, Guangzhi Wang, Zhao Chen, Yang Li, Yan Zhao, Deshun Liu, Huanyu Zhao, Feng Zhang, Jihong Yao and 1 more

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed
9.1field-weighted citation impact, top 1% 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

124 citing papers in PubMed, 236 citations in OpenAlex.

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  6. [SingleZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026
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64 more citing papers are in PubMed but not listed here.

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

11 authors at 2 institutions in 1 country.

Zhanyu WangDepartment of Surgery, The Second Affiliated Hospital of Dalian Medical University, Dalian, 116023, China.
Ruimin SunDepartment of Pharmacology, Dalian Medical University, Dalian, 116044, China.
Guangzhi WangDepartment of Surgery, The Second Affiliated Hospital of Dalian Medical University, Dalian, 116023, China.
Zhao ChenDepartment of Surgery, The Second Affiliated Hospital of Dalian Medical University, Dalian, 116023, China.
Yang LiDepartment of Surgery, The Second Affiliated Hospital of Dalian Medical University, Dalian, 116023, China.
Yan ZhaoDepartment of Pharmacology, Dalian Medical University, Dalian, 116044, China.
Deshun LiuDepartment of Surgery, The Second Affiliated Hospital of Dalian Medical University, Dalian, 116023, China.
Huanyu ZhaoDepartment of Pharmacology, Dalian Medical University, Dalian, 116044, China.
Feng ZhangDepartment of Surgery, The Second Affiliated Hospital of Dalian Medical University, Dalian, 116023, China.
Jihong YaoDepartment of Pharmacology, Dalian Medical University, Dalian, 116044, China. Electronic address: yaojihong65@dmu.edu.cn.
Xiaofeng TianDepartment of Surgery, The Second Affiliated Hospital of Dalian Medical University, Dalian, 116023, China. Electronic address: txfdl@dmu.edu.cn.
Dalian Medical University · CNSecond Affiliated Hospital of Dalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHydrogen peroxide (H

methodsAn intestinal I/R model was established in mice with superior mesenteric artery occlusion, and Caco-2 cells were subjected to hypoxia/reoxygenation (H/R) for the in vivo simulation of I/R.

resultsPRDX3 expression was decreased during intestinal I/R injury, and PRDX3 overexpression significantly attenuated H/R-induced mitochondrial oxidative damage and apoptosis in Caco-2 cells. The level of acetylated PRDX3 was clearly increased both in vivo and in vitro. The inhibition of SIRTs by nicotinamide (NAM) increased the level of acetylated PRDX3 and impaired the antioxidative activity of PRDX3. Furthermore, NAM did not increase the acetylation of PRDX3 in sirtuin-3 (SIRT3)-knockdown Caco-2 cells. Importantly, PRDX3 acetylation was increased in mice lacking SIRT3, and this effect was accompanied by serious mitochondrial oxidative damage, apoptosis and remote organ damage after intestinal I/R injury. We screened potential sites of PRDX3 acetylation in the previously reported acetylproteome through immunoprecipitation (IP) experiments and found that SIRT3 deacetylates K253 on PRDX3 in Caco-2 cells. Furthermore, PRDX3 with the lysine residue K253 mutated to arginine (K253R) increased its dimerization in Caco-2 cells after subjected to 12 h hypoxia and followed 4 h reoxygenation. Caco-2 cells transfected with the K253R plasmid exhibited notably less mitochondrial damage and apoptosis, and transfection of the K253Q plasmid abolished the protective effect of PRDX3 overexpression. Analysis of ischemic intestines from clinical patients further verified the correlation between SIRT3 and PRDX3.

conclusionsPRDX3 is a key protective factor for intestinal I/R injury, and SIRT3-mediated PRDX3 deacetylation can alleviate intestinal I/R-induced mitochondrial oxidative damage and apoptosis.

Indexed as

AcetylationAnimalsApoptosisBiomarkersBiopsyCell Line, TumorCytokinesDisease SusceptibilityIntestinesMaleMiceMice, KnockoutMitochondriaOxidative StressPeroxiredoxin IIIReperfusion InjuryBiomarkersCytokinesPeroxiredoxin IIIPrdx3 protein, mouseSirtuin 3ApoptosisIntestinal ischemia reperfusionMitochondrial oxidative damagePRDX3SIRT3

Identifiers

PMID31655428
PMCPMC6820261
OpenAlexW2980020667

What OpenQuestion holds

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LicenceCC BY
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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.