Evidence map›Paper›PMID 32581828›Full record

ArticleFrontiers in physiology2020

MiR-181d-5p Targets KLF6 to Improve Ischemia/Reperfusion-Induced AKI Through Effects on Renal Function, Apoptosis, and Inflammation.

Yue Zhang, Chenyu Li, Chen Guan, Bin Zhou, Lin Wang, Chengyu Yang, Li Zhen, Jie Dai, Long Zhao, Wei Jiang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

30 citing papers in PubMed, 62 citations in OpenAlex.

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  18. MicroRNAs in kidney injury and disease.Nature reviews. Nephrology · 2022
    Review
  19. Article
  20. 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

11 authors at 2 institutions in 2 countries.

Yue ZhangDepartment of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, China.
Chenyu LiDepartment of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, China.
Chen GuanDepartment of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, China.
Bin ZhouDepartment of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, China.
Lin WangDepartment of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, China.
Chengyu YangDepartment of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, China.
Li ZhenDepartment of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, China.
Jie DaiDepartment of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, China.
Long ZhaoDepartment of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, China.
Wei JiangDepartment of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, China.
Yan XuDepartment of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, China.
Qingdao University · CNAffiliated Hospital of Qingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal tubular epithelial cell (RTEC) death and renal interstitial inflammation are the most crucial pathophysiological changes in acute kidney ischemia/reperfusion injury (IRI). The microRNA (miR)-181d family plays diverse roles in cell proliferation, apoptosis and inflammation, but its renal target and potential role in IRI are unknown. Here, we showed that the expression of miR-181d-5p decreased and Krueppel-like factor 6 (KLF6) increased in a renal cell (HK-2) model of hypoxia/reoxygenation (H/R) injury and a mouse model of renal IRI. They were mainly distributed in the renal tubules. After renal IRI, miR-181d-5p overexpression significantly inhibited inflammatory mediators, reduced apoptosis and further improved renal function. KLF6 exacerbated RTEC damage and acted as a NF-κB co-activator to aggravate the renal IRI inflammatory response. Mechanistically, KLF6 was predicted as a new potential target gene of miR-181d-5p through bioinformatic analysis and luciferase reporter assay verification. After overexpressing miR-181d-5p and inhibiting KLF6, the role of miR-181d-5p was weakened on the renal damage improvement. In conclusion, miR-181d-5p upregulation produced protective antiapoptotic and anti-inflammatory effects against IRI in kidneys

Indexed as

apoptosisinflammationIRIKLF6MiR-181d-5prenal function

Identifiers

PMID32581828
PMCPMC7295155
OpenAlexW3029895181

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.