PDZK1 improves ventricular remodeling in hypertensive rats by regulating the stability of the Mas receptor

IF 3 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Amino Acids Pub Date : 2023-09-11 DOI:10.1007/s00726-023-03331-z
Jinyu Chi, Wanlin Li, Yang Xu, Xiuzhi Li, Xiaohui Zhang, Zhiyu Shi, Chunnan Liu, Wenxiu Liu, Meng Zhao, Yan Meng, Dechao Zhao
{"title":"PDZK1 improves ventricular remodeling in hypertensive rats by regulating the stability of the Mas receptor","authors":"Jinyu Chi,&nbsp;Wanlin Li,&nbsp;Yang Xu,&nbsp;Xiuzhi Li,&nbsp;Xiaohui Zhang,&nbsp;Zhiyu Shi,&nbsp;Chunnan Liu,&nbsp;Wenxiu Liu,&nbsp;Meng Zhao,&nbsp;Yan Meng,&nbsp;Dechao Zhao","doi":"10.1007/s00726-023-03331-z","DOIUrl":null,"url":null,"abstract":"<div><p>Ventricular remodeling is one of the main causes of mortality from heart failure due to hypertension. Exploring its mechanism and finding therapeutic targets have become urgent scientific problems to be solved. A number of studies have shown that Mas, as an Ang-(1-7) specific receptor, was significantly reduced in myocardial tissue of rats undergoing hypertensive ventricular remodeling. It has been reported that Mas receptor levels are significantly downregulated in myocardium undergoing ventricular remodeling, but studies focused on intracellular and post-translational modifications of Mas are lacking. The results of this research are as follows: (1) PDZK1 interacts with the carboxyl terminus of Mas through its PDZ1 domain; (2) the expression of PDZK1 and Mas is decreased in rats undergoing hypertensive ventricular remodeling, and PDZK1 upregulation can ameliorate hypertensive myocardial fibrosis and myocardial hypertrophy; (3) PDZK1 enhances the stability of Mas protein through the proteasome pathway, and the proteasome inhibitor MG132 promotes hypertensive ventricular remodeling. PDZK1 improves ventricular remodeling in hypertensive rats by regulating Mas receptor stability. This study provides a scientific basis for the prevention and treatment of ventricular remodeling.</p></div>","PeriodicalId":7810,"journal":{"name":"Amino Acids","volume":null,"pages":null},"PeriodicalIF":3.0000,"publicationDate":"2023-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Amino Acids","FirstCategoryId":"99","ListUrlMain":"https://link.springer.com/article/10.1007/s00726-023-03331-z","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Ventricular remodeling is one of the main causes of mortality from heart failure due to hypertension. Exploring its mechanism and finding therapeutic targets have become urgent scientific problems to be solved. A number of studies have shown that Mas, as an Ang-(1-7) specific receptor, was significantly reduced in myocardial tissue of rats undergoing hypertensive ventricular remodeling. It has been reported that Mas receptor levels are significantly downregulated in myocardium undergoing ventricular remodeling, but studies focused on intracellular and post-translational modifications of Mas are lacking. The results of this research are as follows: (1) PDZK1 interacts with the carboxyl terminus of Mas through its PDZ1 domain; (2) the expression of PDZK1 and Mas is decreased in rats undergoing hypertensive ventricular remodeling, and PDZK1 upregulation can ameliorate hypertensive myocardial fibrosis and myocardial hypertrophy; (3) PDZK1 enhances the stability of Mas protein through the proteasome pathway, and the proteasome inhibitor MG132 promotes hypertensive ventricular remodeling. PDZK1 improves ventricular remodeling in hypertensive rats by regulating Mas receptor stability. This study provides a scientific basis for the prevention and treatment of ventricular remodeling.

Abstract Image

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
PDZK1通过调节Mas受体的稳定性改善高血压大鼠心室重构。
心室重构是高血压引起心力衰竭死亡的主要原因之一。探索其机制和寻找治疗靶点已成为亟待解决的科学问题。大量研究表明,Mas作为一种Ang-(1-7)特异性受体,在高血压心室重构大鼠心肌组织中显著减少。据报道,在心室重构的心肌中,Mas受体水平显著下调,但缺乏对Mas细胞内和翻译后修饰的研究。本研究结果如下:(1)PDZK1通过其PDZ1结构域与Mas的羧基端相互作用;(2)高血压心室重构大鼠PDZK1和Mas表达降低,PDZK1上调可改善高血压心肌纤维化和心肌肥厚;(3) PDZK1通过蛋白酶体途径增强Mas蛋白的稳定性,蛋白酶体抑制剂MG132促进高血压心室重构。PDZK1通过调节Mas受体稳定性改善高血压大鼠心室重构。本研究为预防和治疗心室重构提供了科学依据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Amino Acids
Amino Acids 生物-生化与分子生物学
CiteScore
6.40
自引率
5.70%
发文量
99
审稿时长
2.2 months
期刊介绍: Amino Acids publishes contributions from all fields of amino acid and protein research: analysis, separation, synthesis, biosynthesis, cross linking amino acids, racemization/enantiomers, modification of amino acids as phosphorylation, methylation, acetylation, glycosylation and nonenzymatic glycosylation, new roles for amino acids in physiology and pathophysiology, biology, amino acid analogues and derivatives, polyamines, radiated amino acids, peptides, stable isotopes and isotopes of amino acids. Applications in medicine, food chemistry, nutrition, gastroenterology, nephrology, neurochemistry, pharmacology, excitatory amino acids are just some of the topics covered. Fields of interest include: Biochemistry, food chemistry, nutrition, neurology, psychiatry, pharmacology, nephrology, gastroenterology, microbiology
期刊最新文献
Identification of amino acids metabolomic profiling in human plasma distinguishes lupus nephritis from systemic lupus erythematosus Evaluation of supplementary carnosine accumulation and distribution: an initial analysis of participants in the Nucleophilic Defense Against PM Toxicity (NEAT) clinical trial. Effect of weight loss interventions on metabolomic signatures in obese children with insulin resistance. Exploring the interplay between kidney function and urinary metabolites in young adults: the African-PREDICT study. N-carboxyacyl and N-α-aminoacyl derivatives of aminoaldehydes as shared substrates of plant aldehyde dehydrogenases 10 and 7.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1