Angiotensin II Causes Biphasic STAT3 Activation Through TLR4 to Initiate Cardiac Remodeling-Reference-Cited by-同舟云学术

Angiotensin II Causes Biphasic STAT3 Activation Through TLR4 to Initiate Cardiac Remodeling

Published:2018-12 Issue:6 Volume:72 Page:1301-1311
ISSN:0194-911X
Container-title:Hypertension
language:en
Short-container-title:Hypertension

Author:

Han Jibo¹²³,Ye Shiju¹²,Zou Chunpeng⁴,Chen Taiwei¹²,Wang Jingying¹,Li Jieli¹,Jiang Liqin³,Xu Jianjiang³,Huang Weijian²,Wang Yi¹,Liang Guang¹

Affiliation:

1. From the Chemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Zhejiang, China (J.H., S.Y., T.C., J.W., J.L., Y.W., G.L.)

2. Department of Cardiology, the First Affiliated Hospital of Wenzhou Medical University, Zhejiang, China (J.H., S.Y., T.C., W.H.)

3. Department of Cardiology, the Second Affiliated Hospital of Jiaxing University, Zhejiang, China (J.H., L.J., J.X.)

4. Department of Ultrasonography, the Second Affiliated Hospital of Wenzhou Medical University, Zhejiang, China (C.Z.).

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Internal Medicine

Reference40 articles.

1. The war against heart failure: the Lancet lecture

2. New Take on the Role of Angiotensin II in Cardiac Hypertrophy and Fibrosis

3. MD2 mediates angiotensin II-induced cardiac inflammation and remodeling via directly binding to Ang II and activating TLR4/NF-κB signaling pathway

4. The role of mAKAPβ in the process of cardiomyocyte hypertrophy induced by angiotensin II

5. Intracellular Angiotensin II Production in Diabetic Rats Is Correlated With Cardiomyocyte Apoptosis, Oxidative Stress, and Cardiac Fibrosis

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