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


Journal

Communications biology
ISSN: 2399-3642
Titre abrégé: Commun Biol
Pays: England
ID NLM: 101719179

Informations de publication

Date de publication:
24 06 2020
Historique:
received: 22 10 2019
accepted: 08 06 2020
entrez: 26 6 2020
pubmed: 26 6 2020
medline: 24 6 2021
Statut: epublish

Résumé

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.

Identifiants

pubmed: 32581266
doi: 10.1038/s42003-020-1058-2
pii: 10.1038/s42003-020-1058-2
pmc: PMC7314757
doi:

Substances chimiques

MIRN135 microRNA, human 0
MicroRNAs 0
Receptors, Cytoplasmic and Nuclear 0
farnesoid X-activated receptor 0C5V0MRU6P
MAP Kinase Kinase Kinases EC 2.7.11.25
MAP kinase kinase kinase 7 EC 2.7.11.25
Receptor, Transforming Growth Factor-beta Type I EC 2.7.11.30
TGFBR1 protein, human EC 2.7.11.30

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

327

Commentaires et corrections

Type : ErratumIn

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Auteurs

Chao Li (C)

Experimental Center, Shandong University of Traditional Chinese Medicine, Jinan, 250355, China.
Department of Clinical Pharmacology and Toxicology, University Hospital Zurich, Zurich, 8032, Switzerland.

Shijun Zhang (S)

Experimental Center, Shandong University of Traditional Chinese Medicine, Jinan, 250355, China.

Xiaoqing Chen (X)

Experimental Center, Shandong University of Traditional Chinese Medicine, Jinan, 250355, China.

Jingkang Ji (J)

Experimental Center, Shandong University of Traditional Chinese Medicine, Jinan, 250355, China.

Wenqing Yang (W)

Experimental Center, Shandong University of Traditional Chinese Medicine, Jinan, 250355, China.

Ting Gui (T)

Experimental Center, Shandong University of Traditional Chinese Medicine, Jinan, 250355, China.

Zhibo Gai (Z)

Experimental Center, Shandong University of Traditional Chinese Medicine, Jinan, 250355, China. gaizhibo@gamil.com.
Department of Clinical Pharmacology and Toxicology, University Hospital Zurich, Zurich, 8032, Switzerland. gaizhibo@gamil.com.

Yunlun Li (Y)

Experimental Center, Shandong University of Traditional Chinese Medicine, Jinan, 250355, China. yunlun.lee@hotmail.com.
Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, 250000, China. yunlun.lee@hotmail.com.

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