Evidence map›Paper›PMID 30941422›Full record

ArticleJournal of molecular cell biology2020

miR-145 improves metabolic inflammatory disease through multiple pathways.

Min He, Nan Wu, Man Cheong Leong, Weiwei Zhang, Zi Ye, Rumei Li, Jinyang Huang, Zhaoyun Zhang, Lianxi Li, Xiao Yao and 14 more

Open access · goldAbstract read
In one paragraph

Article in Journal of molecular cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

35 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. [miRNA Is Involved in the Pathogenesis of Multiple Diseases by Targeting Osteoprotegerin].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2024
    Review
  11. Article
  12. International journal of molecular sciences · 2023
    Article
  13. Article
  14. Article
  15. MicroRNAs Contribute to Host Response toInfection and immunity · 2023
    Article
  16. Review
  17. Article
  18. Annals of translational medicine · 2022
    Article
  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

24 authors at 2 institutions in 2 countries.

Min HeDepartment of Endocrinology and Metabolism, Huashan Hospital, Shanghai Medical College, Institute of Endocrinology and Diabetology, Fudan University, Shanghai, China.
Nan WuDepartment of Endocrinology and Metabolism, Huashan Hospital, Shanghai Medical College, Institute of Endocrinology and Diabetology, Fudan University, Shanghai, China.
Man Cheong LeongDepartment of Endocrinology and Metabolism, Huashan Hospital, Shanghai Medical College, Institute of Endocrinology and Diabetology, Fudan University, Shanghai, China.
Weiwei ZhangDepartment of Endocrinology and Metabolism, Huashan Hospital, Shanghai Medical College, Institute of Endocrinology and Diabetology, Fudan University, Shanghai, China.
Zi YeDepartment of Endocrinology and Metabolism, Huashan Hospital, Shanghai Medical College, Institute of Endocrinology and Diabetology, Fudan University, Shanghai, China.
Rumei LiDepartment of Endocrinology and Metabolism, Huashan Hospital, Shanghai Medical College, Institute of Endocrinology and Diabetology, Fudan University, Shanghai, China.
Jinyang HuangDepartment of Endocrinology and Metabolism, Huashan Hospital, Shanghai Medical College, Institute of Endocrinology and Diabetology, Fudan University, Shanghai, China.
Zhaoyun ZhangDepartment of Endocrinology and Metabolism, Huashan Hospital, Shanghai Medical College, Institute of Endocrinology and Diabetology, Fudan University, Shanghai, China.
Lianxi LiDepartment of Endocrinology and Metabolism, Huashan Hospital, Shanghai Medical College, Institute of Endocrinology and Diabetology, Fudan University, Shanghai, China.
Xiao YaoDepartment of Endocrinology and Metabolism, Huashan Hospital, Shanghai Medical College, Institute of Endocrinology and Diabetology, Fudan University, Shanghai, China.
Wenbai ZhouDepartment of Endocrinology and Metabolism, Huashan Hospital, Shanghai Medical College, Institute of Endocrinology and Diabetology, Fudan University, Shanghai, China.
Naijia LiuDepartment of Endocrinology and Metabolism, Huashan Hospital, Shanghai Medical College, Institute of Endocrinology and Diabetology, Fudan University, Shanghai, China.
Zhihong YangDepartment of Endocrinology and Metabolism, Huashan Hospital, Shanghai Medical College, Institute of Endocrinology and Diabetology, Fudan University, Shanghai, China.
Xuehong DongDepartment of Endocrinology and Metabolism, Huashan Hospital, Shanghai Medical College, Institute of Endocrinology and Diabetology, Fudan University, Shanghai, China.
Yintao LiDepartment of Endocrinology and Metabolism, Huashan Hospital, Shanghai Medical College, Institute of Endocrinology and Diabetology, Fudan University, Shanghai, China.
Lili ChenDepartment of Endocrinology and Metabolism, Huashan Hospital, Shanghai Medical College, Institute of Endocrinology and Diabetology, Fudan University, Shanghai, China.
Qin LiDepartment of Endocrinology and Metabolism, Huashan Hospital, Shanghai Medical College, Institute of Endocrinology and Diabetology, Fudan University, Shanghai, China.
Xuanchun WangDepartment of Endocrinology and Metabolism, Huashan Hospital, Shanghai Medical College, Institute of Endocrinology and Diabetology, Fudan University, Shanghai, China.
Jie WenDepartment of Endocrinology and Metabolism, Huashan Hospital, Shanghai Medical College, Institute of Endocrinology and Diabetology, Fudan University, Shanghai, China.
Xiaolong ZhaoDepartment of Endocrinology and Metabolism, Huashan Hospital, Shanghai Medical College, Institute of Endocrinology and Diabetology, Fudan University, Shanghai, China.
Bin LuDepartment of Endocrinology and Metabolism, Huashan Hospital, Shanghai Medical College, Institute of Endocrinology and Diabetology, Fudan University, Shanghai, China.
Yehong YangDepartment of Endocrinology and Metabolism, Huashan Hospital, Shanghai Medical College, Institute of Endocrinology and Diabetology, Fudan University, Shanghai, China.
Qinghua WangDepartment of Endocrinology and Metabolism, Huashan Hospital, Shanghai Medical College, Institute of Endocrinology and Diabetology, Fudan University, Shanghai, China.
Renming HuDepartment of Endocrinology and Metabolism, Huashan Hospital, Shanghai Medical College, Institute of Endocrinology and Diabetology, Fudan University, Shanghai, China.
Fudan University · CNHuashan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic inflammation plays a pivotal role in insulin resistance and type 2 diabetes, yet the mechanisms are not completely understood. Here, we demonstrated that serum LPS levels were significantly higher in newly diagnosed diabetic patients than in normal control. miR-145 level in peripheral blood mononuclear cells decreased in type 2 diabetics. LPS repressed the transcription of miR-143/145 cluster and decreased miR-145 levels. Attenuation of miR-145 activity by anti-miR-145 triggered liver inflammation and increased serum chemokines in C57BL/6 J mice. Conversely, lentivirus-mediated miR-145 overexpression inhibited macrophage infiltration, reduced body weight, and improved glucose metabolism in db/db mice. And miR-145 overexpression markedly reduced plaque size in the aorta in ApoE-/- mice. Both OPG and KLF5 were targets of miR-145. miR-145 repressed cell proliferation and induced apoptosis partially by targeting OPG and KLF5. miR-145 also suppressed NF-κB activation by targeting OPG and KLF5. Our findings provide an association of the environment with the progress of metabolic disorders. Increasing miR-145 may be a new potential therapeutic strategy in preventing and treating metabolic diseases such as type 2 diabetes and atherosclerosis.

Indexed as

AnimalsApoptosisAtherosclerosisDiabetes Mellitus, Type 2Disease Models, AnimalDown-RegulationGenetic VectorsGlucoseGlucose IntoleranceHEK293 CellsHumansLeukocytes, MononuclearMacrophagesMaleMiceMice, Inbred C57BLGlucoseMicroRNAsMIRN145a microRNA, mouseMIRN145 microRNA, humanOligonucleotides, AntisenseKruppel-like factor 5monocyteNF-κBosteoprotegerintype 2 diabetes

Identifiers

PMID30941422
PMCPMC7109608
OpenAlexW2930072174

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.