Evidence map›Paper›PMID 29849933›Full record

ArticleOncotarget2018

Rotenone ameliorates chronic renal injury caused by acute ischemia/reperfusion.

Wen Zhang, Yugen Sha, Ke Wei, Chunfeng Wu, Dan Ding, Yunwen Yang, Chunhua Zhu, Yue Zhang, Guixia Ding, Aihua Zhang and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 26 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

12 authors at 2 institutions in 1 country.

Wen ZhangDepartment of Nephrology, Children's Hospital of Nanjing Medical University, Nanjing 210008, China.
Yugen ShaDepartment of Nephrology, Children's Hospital of Nanjing Medical University, Nanjing 210008, China.
Ke WeiDepartment of Nephrology, Children's Hospital of Nanjing Medical University, Nanjing 210008, China.
Chunfeng WuDepartment of Nephrology, Children's Hospital of Nanjing Medical University, Nanjing 210008, China.
Dan DingDepartment of Nephrology, Children's Hospital of Nanjing Medical University, Nanjing 210008, China.
Yunwen YangDepartment of Nephrology, Children's Hospital of Nanjing Medical University, Nanjing 210008, China.
Chunhua ZhuDepartment of Nephrology, Children's Hospital of Nanjing Medical University, Nanjing 210008, China.
Yue ZhangDepartment of Nephrology, Children's Hospital of Nanjing Medical University, Nanjing 210008, China.
Guixia DingDepartment of Nephrology, Children's Hospital of Nanjing Medical University, Nanjing 210008, China.
Aihua ZhangDepartment of Nephrology, Children's Hospital of Nanjing Medical University, Nanjing 210008, China.
Zhanjun JiaDepartment of Nephrology, Children's Hospital of Nanjing Medical University, Nanjing 210008, China.
Songming HuangDepartment of Nephrology, Children's Hospital of Nanjing Medical University, Nanjing 210008, China.
Second Affiliated Hospital of Nanjing Medical University · CNNanjing University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute kidney injury (AKI) has been widely recognized as an important risk factor leading to the occurrence and progression of chronic kidney disease (CKD). Thus, development of the strategies in retarding the transition of AKI to CKD is becoming a hot research field. Recently, accumulating evidence suggested a pathogenic role of mitochondrial dysfunction in both AKI and CKD. Therefore, in the present study, we evaluated the effect of mitochondrial complex 1 inhibition by rotenone on the chronic renal damage induced by acute ischemia-reperfusion. The mice were treated with 45 min unilateral renal ischemia and reperfusion (I/R) to induce an acute renal injury. After three days of I/R injury, rotenone at a dose of 200 ppm in food was administered to the mice. Strikingly, after three weeks treatment with rotenone, we found that the unilateral I/R-induced tubular damage, tubulointerstitial fibrosis were all attenuated by rotenone as determined by the tubular injury score, Masson staining, and the levels of collagen-I, collagen-III, fibronectin, PAI-1, and TGF-β. Meanwhile, the enhanced inflammatory markers of TNF-α, IL-1β, IL-6, and IL-18 and apoptotic markers of Bax and caspase-3 were all significantly blunted by inhibiting mitochondrial complex-1. Moreover, rotenone treatment also partially protected the mitochondria as shown by the restoration of mitochondrial SOD (SOD2), ATPB, and mitochondrial DNA copy number. These findings suggested that inhibition of mitochondrial complex-1 activity by rotenone could retard the progression of AKI to CKD probably via protecting the mitochondrial function to some extent.

Indexed as

AKICKDmitochondriarotenone

Identifiers

PMID29849933
PMCPMC5966262
OpenAlexW2802634314

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.