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Elabela alleviates ferroptosis, myocardial remodeling, fibrosis and heart dysfunction in hypertensive mice by modulating the IL-6/STAT3/GPX4 signaling
In conclusion, elabela antagonizes Ang II-mediated promotion of CMVECs ferroptosis, adverse myocardial remodeling, fibrosis and heart dysfunction through modulating the IL-6/STAT3/GPX4 signaling pathway. Targeting elabela-APJ axis serves as a novel strategy for hypertensive heart diseases.PMID:35122997 | DOI:10.1016/j.freeradbiomed.2022.01.020
Source: Free Radical Biology and Medicine - February 5, 2022 Category: Biology Authors: Zhenzhou Zhang Jianqiong Tang Jiawei Song Mengshi Xie Ying Liu Zhaojie Dong Xiaoyan Liu Xueting Li Miwen Zhang Yihang Chen Hongyu Shi Jiuchang Zhong Source Type: research

LRRC8A contributes to angiotensin II-induced cardiac hypertrophy by interacting with NADPH oxidases via the C-terminal leucine-rich repeat domain.
Abstract Cardiac hypertrophy, an important cause of heart failure, is characterized by an increase in heart weight, the ventricular wall, and cardiomyocyte volume. The volume regulatory anion channel (VRAC) is an important regulator of cell volume. However, its role in cardiac hypertrophy remains unclear. The purpose of this study was to investigate the effect of leucine-rich repeat-containing 8A (LRRC8A), an essential component of the VRAC, on angiotensin II (AngII)-induced cardiac hypertrophy. Our results showed that LRRC8A expression, NADPH oxidase activity, and reactive oxygen species (ROS) production were inc...
Source: Free Radical Biology and Medicine - January 27, 2021 Category: Biology Authors: Huo C, Liu Y, Li X, Xu R, Jia X, Hou L, Wang X Tags: Free Radic Biol Med Source Type: research

Transmembrane tumor necrosis factor alpha attenuates pressure-overload cardiac hypertrophy via tumor necrosis factor receptor 2
by Kun Miao, Ling Zhou, Hongping Ba, Chenxi Li, Haiyan Gu, Bingjiao Yin, Jing Wang, Xiang-ping Yang, Zhuoya Li, Dao Wen Wang Tumor necrosis factor-alpha (TNF-α) plays an important pathogenic role in cardiac hypertrophy and heart failure (HF); however, anti-TNF is paradoxically negative in clinical trials and even worsens HF, indicating a possible protective role of TNF-α in HF. TNF-α exists in transmembrane (tmTNF-α ) and soluble (sTNF-α) forms. Herein, we found that TNF receptor 1 (TNFR1) knockout (KO) or knockdown (KD) by short hairpin RNA or small interfering RNA (siRNA) significantly alleviated cardiac hypertroph...
Source: PLoS Biology: Archived Table of Contents - December 3, 2020 Category: Biology Authors: Kun Miao Source Type: research

The activation of the G protein-coupled estrogen receptor (GPER) prevents and regresses cardiac hypertrophy
Publication date: Available online 28 December 2019Source: Life SciencesAuthor(s): Romina A. Di Mattia, Juan I.E. Mariángelo, Paula G. Blanco, Carolina Jaquenod De Giusti, Enrique L. Portiansky, Cecilia B. Mundiña-Weilenmann, Ernesto A. Aiello, Alejandro OrlowskiAbstractVentricular hypertrophy is a risk factors for arrhythmias, ischemia and sudden death. It involves cellular modifications leading to a pathological remodeling and is associated with heart failure. The activation of the G protein-coupled estrogen receptor (GPER) mediates beneficial actions in the cardiovascular system. Our goal was to prevent and regress th...
Source: Life Sciences - December 30, 2019 Category: Biology Source Type: research

MicroRNA-92b-3p suppresses angiotensin II-induced cardiomyocyte hypertrophy via targeting HAND2
In this study, we want to investigate the role of microRNA-92b-3p (miR-92b-3p) in cardiomyocyte hypertrophy and the mechanisms involved.Materials and methodsNeonatal mouse ventricular cells (NMVCs) were isolated from the hearts of 1–3-d-old newborn C57BL6 mice. The isolated NMVCs were induced hypertrophic phenotype by Angiotensin-II (Ang-II) and the cell size was examined by FITC-phalloidin staining assay. The expression of miR-92b-3p was determined by quantitative real-time PCR (qRT-qPCR). MRNA and protein level of β-MHC, ACTA1 and HAND2 in NMVCs transfected with miR-92b-3p mimic and inhibition were assessed by RT-qPCR...
Source: Life Sciences - July 6, 2019 Category: Biology Source Type: research

C1QTNF1 attenuates angiotensin II-induced cardiac hypertrophy via activation of the AMPKa pathway.
CONCLUSION: Our results demonstrated that C1QTNF1 improves cardiac function and inhibits cardiac hypertrophy and fibrosis by increasing and activating AMPKa, suggesting that C1QTNF1 could be a therapeutic target for cardiac hypertrophy and heart failure. PMID: 29733904 [PubMed - as supplied by publisher]
Source: Free Radical Biology and Medicine - May 4, 2018 Category: Biology Authors: Wu L, Gao L, Zhang D, Yao R, Huang Z, Du B, Wang Z, Xiao L, Li P, Li Y, Liang C, Zhang Y Tags: Free Radic Biol Med Source Type: research