兰州大学机构库
RBM25 regulates hypoxic cardiomyocyte apoptosis through CHOP-associated endoplasmic reticulum stress
Zhu, Ziwei1; Pu, Jie1; Li, Yongnan2; Chen, Jianshu1; Ding, Hong1; Zhou, Anyu3; Zhang, Xiaowei1
2023-09-22
Online publication date2023-09
Source PublicationCELL STRESS & CHAPERONES   Impact Factor & Quartile
ISSN1355-8145 ; 1466-1268
page numbers16
AbstractIschemic heart failure (HF) is one of the leading causes of global morbidity and mortality; blocking the apoptotic cascade could help improve adverse outcomes of it. RNA-binding motif protein 25 (RBM25) is an RNA-binding protein related to apoptosis; however, its role remains unknown in ischemic HF. The main purpose of this study is to explore the mechanism of RBM25 in ischemic HF. Establishing an ischemic HF model and oxygen-glucose deprivation (OGD) model. ELISA was performed to evaluate the BNP level in the ischemic HF model. Echocardiography and histological analysis were performed to assess cardiac function and infarct size. Proteins were quantitatively and locationally analyzed by western blotting and immunofluorescence. The morphological changes of endoplasmic reticulum (ER) were observed with ER-tracker. Cardiac function and myocardial injury were observed in ischemic HF rats. RBM25 was elevated in cardiomyocytes of hypoxia injury hearts and localized in nucleus both in vitro and in vivo. In addition, cell apoptosis was significantly increased when overexpressed RBM25. Moreover, ER stress stimulated upregulation of RBM25 and promoted cell apoptosis through the CHOP related pathway. Finally, inhibiting the expression of RBM25 could ameliorate the apoptosis and improve cardiac function through blocking the activation of CHOP signaling pathway. RBM25 is significantly upregulated in ischemic HF rat heart and OGD model, which leads to apoptosis by modulating the ER stress through CHOP pathway. Knockdown of RBM25 could reverse apoptosis-mediated cardiac dysfunction. RBM25 may be a promising target for the treatment of ischemic HF.
KeywordIschemic heart failure Myocardial infarction Apoptosis Endoplasmic reticulum stress RBM25
PublisherSPRINGER
DOI10.1007/s12192-023-01380-7
Indexed BySCIE
Language英语
WOS Research AreaCell Biology
WOS SubjectCell Biology
WOS IDWOS:001068486200001
Original Document TypeArticle ; Early Access
PMID 3773686
Citation statistics
Document Type期刊论文
Identifierhttps://ir.lzu.edu.cn/handle/262010/569251
Collection兰州大学
Corresponding AuthorZhang, Xiaowei
Affiliation
1.Lanzhou Univ, Dept Cardiovasc Med, Hosp 2, Lanzhou 730000, Peoples R China;
2.Lanzhou Univ, Dept Pathol, Hosp 2, Lanzhou 730000, Peoples R China;
3.Brown Univ, Dept Dermatol, Warren Alpert Med Sch, Providence, RI USA
Recommended Citation
GB/T 7714
Zhu, Ziwei,Pu, Jie,Li, Yongnan,et al. RBM25 regulates hypoxic cardiomyocyte apoptosis through CHOP-associated endoplasmic reticulum stress[J]. CELL STRESS & CHAPERONES,2023.
APA Zhu, Ziwei.,Pu, Jie.,Li, Yongnan.,Chen, Jianshu.,Ding, Hong.,...&Zhang, Xiaowei.(2023).RBM25 regulates hypoxic cardiomyocyte apoptosis through CHOP-associated endoplasmic reticulum stress.CELL STRESS & CHAPERONES.
MLA Zhu, Ziwei,et al."RBM25 regulates hypoxic cardiomyocyte apoptosis through CHOP-associated endoplasmic reticulum stress".CELL STRESS & CHAPERONES (2023).
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