Evidence map›Paper›PMID 32581266›Full record

ArticleCommunications biology2020

Farnesoid X receptor activation inhibits TGFBR1/TAK1-mediated vascular inflammation and calcification via miR-135a-5p.

Chao Li, Shijun Zhang, Xiaoqing Chen, Jingkang Ji, Wenqing Yang, Ting Gui, Zhibo Gai, Yunlun Li

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Communications biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

15 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. TAK1 in Vascular Signaling: "Friend or Foe"?Journal of inflammation research · 2024
    Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Roles of Nuclear Receptors in Vascular Calcification.International journal of molecular sciences · 2021
    Review
  15. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 2 countries.

Chao LiExperimental Center, Shandong University of Traditional Chinese Medicine, Jinan, 250355, China.
Shijun ZhangExperimental Center, Shandong University of Traditional Chinese Medicine, Jinan, 250355, China.
Xiaoqing ChenExperimental Center, Shandong University of Traditional Chinese Medicine, Jinan, 250355, China.
Jingkang JiExperimental Center, Shandong University of Traditional Chinese Medicine, Jinan, 250355, China.
Wenqing YangExperimental Center, Shandong University of Traditional Chinese Medicine, Jinan, 250355, China.
Ting GuiExperimental Center, Shandong University of Traditional Chinese Medicine, Jinan, 250355, China.
Zhibo GaiExperimental Center, Shandong University of Traditional Chinese Medicine, Jinan, 250355, China. gaizhibo@gamil.com.ORCID http://orcid.org/0000-0003-1673-6541
Yunlun LiExperimental Center, Shandong University of Traditional Chinese Medicine, Jinan, 250355, China. yunlun.lee@hotmail.com.ORCID http://orcid.org/0000-0002-2129-1447
Shandong University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic inflammation plays a crucial role in vascular calcification. However, only a few studies have revealed the mechanisms underlying the development of inflammation under high-phosphate conditions in chronic kidney disease (CKD) patients. Here, we show that inflammation resulting from the activation of the TGFBR1/TAK1 pathway is involved in calcification in CKD rats or osteogenic medium-cultured human aortic smooth muscle cells (HASMCs). Moreover, miR-135a-5p is demonstrated to be a key regulator of the TGFBR1/TAK1 pathway, which has been reported to be decreased in CKD rats. We further reveal that farnesoid X receptor (FXR) activation increases miR-135a-5p expression, thereby inhibiting the activation of the TGFBR1/TAK1 pathway, ultimately resulting in the attenuation of vascular inflammation and calcification in CKD rats. Our findings provide advanced insights into the mechanisms underlying the development of inflammation in vascular calcification, and evidence that FXR activation could serve as a therapeutic strategy for retarding vascular calcification in CKD patients.

Indexed as

AnimalsAortaCalcinosisCells, CulturedFemaleHumansMaleMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMicroRNAsMuscle, Smooth, VascularOsteogenesisRats, WistarReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearReceptor, Transforming Growth Factor-beta Type IMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMicroRNAsMIRN135 microRNA, humanReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearReceptor, Transforming Growth Factor-beta Type ITGFBR1 protein, human

Identifiers

PMID32581266
PMCPMC7314757
OpenAlexW3038082809

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.