Evidence map›Paper›PMID 31949789›Full record

ArticleInternational journal of clinical and experimental pathology2018

Downregulation of miR-181a alleviates renal fibrosis in diabetic nephropathy mice.

Jia Zhang, Cong Wu, Jie Dong, Jian Liu, Xiaowen Wei

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2018. 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
–field-weighted citation impact, top 79% 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. Unraveling the role of MiR-181 in skin fibrosis pathogenesis by targeting NUDT21.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    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

5 authors at 1 institution in 1 country.

Jia ZhangSchool of Medicine, Shandong University Jinan 250012, China.
Cong WuDepartment of Geriatric Endocrinology, The First Affiliated Hospital of Zhengzhou University Zhengzhou 450003, China.
Jie DongDepartment of Geriatric Endocrinology, The First Affiliated Hospital of Zhengzhou University Zhengzhou 450003, China.
Jian LiuZhengzhou University Zhengzhou 450001, China.
Xiaowen WeiDepartment of Geriatric Endocrinology, The First Affiliated Hospital of Zhengzhou University Zhengzhou 450003, China.
Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence suggests that microRNAs are important regulators in the pathology of diabetes and its relevant renal injures. Little is known about the role of miR-181a in development of diabetic nephropathy. The aim of our present study was to investigate levels of miR-181a in diabetic nephropathy and explore its underlying mechanism. In the present study, Db/db and db/m mice were randomized into groups with 12 mice in each: db/m group, db/db group, and antagomiR-181a-treated db/db group. Changes in renal cortical sections were studied by histopathology. Mouse mesangial cells transfected with miR-mimic or miR-inhibitor and cell growth was measured using MTT assay. Levels of miR-181a expression were detected using qRT-PCR under different conditions. Indexes were measured using qRT-PCR and Western blot. Our results show that downregulation of miR-181a could alleviate pathological changes of diabetic nephropathy in mice. miR-181a expression was significantly upregulated in mouse mesaginal cells

Indexed as

Diabetic nephropathymiR-181amouse mesangial cells

Identifiers

PMID31949789
PMCPMC6962790
OpenAlexW3026414650

What OpenQuestion holds

Textmetadata
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.