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Elabela blunts doxorubicin-induced oxidative stress and ferroptosis in rat aortic adventitial fibroblasts by activating the KLF15/GPX4 signaling

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收录情况： ◇ SCIE

作者：
Zhang Mi-Wen[1,2,3] * ; Li Xue-Ting[1,2,3] ; Zhang Zhen-Zhou[1,3] ; Liu Ying[1,3] ; Song Jia-Wei[1,2,3] ; Liu Xin-Ming[1,3] ; Chen Yi-Hang[1,3] ; Wang Ning[4] ; Guo Ying[4] ; Liang Li-Rong[2] ; Zhong Jiu-Chang[1,2,3] ;
机构： [1]Heart Center and Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing, 100020, China. [2]Medical Research Center, Beijing Institute of Respiratory Medicine and Beijing Chaoyang Hospital, Capital Medical University, Beijing, China. [3]Department of Cardiology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, 100020, China. [4]Department of Geratology, Beijing Tongren Hospital, Capital Medical University, Beijing, China
出处：
DOI： 10.1007/s12192-022-01317-6
ISSN：

关键词： Doxorubicin Elabela Oxidative stress Ferroptosis Aortic adventitial fibroblast

摘要：
Doxorubicin (DOX) is a chemotherapeutic drug for a variety of malignancies, while its application is restricted by the cardiovascular toxic effects characterized by oxidative stress. Ferroptosis is a novel iron-dependent regulated cell death driven by lipid peroxidation. Our study aimed to investigate the role of Elabela (ELA) in DOX-induced oxidative stress and ferroptosis. In cultured rat aortic adventitial fibroblasts (AFs), stimulation with DOX dramatically induced cytotoxicity with reduced cell viability and migration ability, and enhanced lactate dehydrogenase (LDH) activity. Importantly, ELA and ferrostatin-1 (Fer-1) mitigated DOX-mediated augmentation of reactive oxygen species (ROS) in rat aortic AFs, accompanied by upregulated levels of Nrf2, SLC7A11, GPX4, and GSH. In addition, ELA reversed DOX-induced dysregulation of apoptosis- and inflammation-related factors including Bax, Bcl2, interleukin (IL)-1β, IL6, IL-10, and CXCL1. Intriguingly, knockdown of Krüppel-like factor 15 (KLF15) by siRNA abolished ELA-mediated alleviation of ROS production and inflammatory responses. More importanly, KLF15 siRNA impeded the beneficial roles of ELA in DOX-pretreated rat aortic AFs by suppressing the Nrf2/SLC7A11/GPX4 signaling. In conclusion, ELA prevents DOX-triggered promotion of cytotoxicity, and exerts anti-oxidative and anti-ferroptotic effects in rat aortic AFs via activation of the KLF15/GPX4 signaling, indicating a promising therapeutic value of ELA in antagonizing DOX-mediated cardiovascular abnormality and disorders.© 2022. The Author(s), under exclusive licence to Cell Stress Society International.

基金：
General Program and the National Major Research Plan Training Program of the National Natural Science Foundation of China (No. 92168117; 81770253; 91849111), Beijing Natural Science Foundation (7222068), Clinical Research Incubation Program of Beijing Chaoyang Hospital Affiliated to Capital Medical University (CYFH202209) and Reform and Development Program of Beijing Institute of Respiratory Medicine (ysrh2022002).
语种：
外文
被引次数：
WOS：
PubmedID：
中科院(CAS)分区：
出版当年[2022]版：
大类 | 3 区 生物学
小类 | 4 区 细胞生物学
最新[2023]版：
大类 | 3 区 生物学
小类 | 3 区 细胞生物学
JCR分区：
出版当年[2021]版：
Q3 CELL BIOLOGY
最新[2023]版：
Q3 CELL BIOLOGY

影响因子： 最新[2023版] 最新五年平均 出版当年[2021版] 出版当年五年平均 出版前一年[2020版] 出版后一年[2022版]

第一作者：
第一作者机构： [1]Heart Center and Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing, 100020, China. [2]Medical Research Center, Beijing Institute of Respiratory Medicine and Beijing Chaoyang Hospital, Capital Medical University, Beijing, China. [3]Department of Cardiology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, 100020, China.
通讯作者：
通讯机构： [1]Heart Center and Beijing Key Laboratory of Hypertension, Beijing Chaoyang Hospital, Capital Medical University, Beijing, 100020, China. [2]Medical Research Center, Beijing Institute of Respiratory Medicine and Beijing Chaoyang Hospital, Capital Medical University, Beijing, China. [3]Department of Cardiology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, 100020, China.
推荐引用方式(GB/T 7714)：
Zhang Mi-Wen,Li Xue-Ting,Zhang Zhen-Zhou,et al.Elabela blunts doxorubicin-induced oxidative stress and ferroptosis in rat aortic adventitial fibroblasts by activating the KLF15/GPX4 signaling[J].CELL STRESS & CHAPERONES.2023,28(1):91-103.doi:10.1007/s12192-022-01317-6.
APA：
Zhang Mi-Wen,Li Xue-Ting,Zhang Zhen-Zhou,Liu Ying,Song Jia-Wei...&Zhong Jiu-Chang.(2023).Elabela blunts doxorubicin-induced oxidative stress and ferroptosis in rat aortic adventitial fibroblasts by activating the KLF15/GPX4 signaling.CELL STRESS & CHAPERONES,28,(1)
MLA：
Zhang Mi-Wen,et al."Elabela blunts doxorubicin-induced oxidative stress and ferroptosis in rat aortic adventitial fibroblasts by activating the KLF15/GPX4 signaling".CELL STRESS & CHAPERONES 28..1(2023):91-103

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