Fibroblast growth factor 21 attenuates salt-sensitive hypertension-induced nephropathy through anti-inflammation and anti-oxidation mechanism

doi:10.1186/s10020-021-00408-x

科研成果详情

题名	Fibroblast growth factor 21 attenuates salt-sensitive hypertension-induced nephropathy through anti-inflammation and anti-oxidation mechanism
作者	Weng, Hua-Chun 1; Lu, Xin-Yu 3; Xu, Yu-Peng 3; Wang, Yi-Hong2; Wang, Dan 2; Feng, Yi-Ling 2; Chi, Zhang 4; Yan, Xiao-Qing4; Lu, Chao-Sheng2; Wang, Hong-Wei 5
发表日期	2021-12
发表期刊	MOLECULAR MEDICINE 影响因子和分区
语种	英语
原始文献类型	Article
关键词	Hypertension Renal injury Fibroblast growth factor 21 AMPK
其他关键词	OXIDATIVE STRESS ; ENDOTHELIAL FUNCTION ; METABOLISM ; PROTECTION ; OUTCOMES ; DISEASE ; GLUCOSE ; FGF21 ; NRF2
摘要	Background Patients with salt-sensitive hypertension are often accompanied with severe renal damage and accelerate to end-stage renal disease, which currently lacks effective treatment. Fibroblast growth factor 21 (FGF21) has been shown to suppress nephropathy in both type 1 and type 2 diabetes mice. Here, we aimed to investigate the therapeutic effect of FGF21 in salt-sensitive hypertension-induced nephropathy. Methods Changes of FGF21 expression in deoxycorticosterone acetate (DOCA)-salt-induced hypertensive mice were detected. The influence of FGF21 knockout in mice on DOCA-salt-induced nephropathy were determined. Recombinant human FGF21 (rhFGF21) was intraperitoneally injected into DOCA-salt-induced nephropathy mice, and then the inflammatory factors, oxidative stress levels and kidney injury-related indicators were observed. In vitro, human renal tubular epithelial cells (HK-2) were challenged by palmitate acid (PA) with or without FGF21, and then changes in inflammation and oxidative stress indicators were tested. Results We observed significant elevation in circulating levels and renal expression of FGF21 in DOCA-salt-induced hypertensive mice. We found that deletion of FGF21 in mice aggravated DOCA-salt-induced nephropathy. Supplementation with rhFGF21 reversed DOCA-salt-induced kidney injury. Mechanically, rhFGF21 induced AMPK activation in DOCA-salt-treated mice and PA-stimulated HK-2 cells, which inhibited NF-kappa B-regulated inflammation and Nrf2-mediated oxidative stress and thus, is important for rhFGF21 protection against DOCA-salt-induced nephropathy. Conclusion These findings indicated that rhFGF21 could be a promising pharmacological strategy for the treatment of salt-sensitive hypertension-induced nephropathy.
资助项目	National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [82170728, 82070834, 82073843]; Natural Science Foundation of Zhejiang provinceNatural Science Foundation of Zhejiang Province [LY19H05001]
出版者	SPRINGER
出版地	NEW YORK
ISSN	1076-1551
EISSN	1528-3658
卷号	27 期号:1 页码:147
DOI	10.1186/s10020-021-00408-x
页数	18
WOS类目	Biochemistry & Molecular Biology ; Cell Biology ; Medicine, Research & Experimental
WOS研究方向	Biochemistry & Molecular Biology ; Cell Biology ; Research & Experimental Medicine
WOS记录号	WOS:000718107000002
收录类别	SCIE ; PUBMED ; SCOPUS
URL	查看原文
PubMed ID	34773993
PMC记录号	PMC8590333
SCOPUSEID	2-s2.0-85119054295
通讯作者地址	[Lu, Chao-Sheng]Department of Pediatrics,The First Affiliated Hospital of Wenzhou Medical University,322 Nanbaixiang Street,Wenzhou,325000,China ; [Wang, Hong-Wei]Key Laboratory of Diagnosis and Treatment of Severe Hepato-Pancreatic Diseases of Zhejiang Province,The First Affiliated Hospital of Wenzhou Medical University,322 Nanbaixiang Street,Wenzhou,325000,China
Scopus学科分类	Molecular Medicine;Molecular Biology;Genetics;Genetics (clinical)
引用统计	被引频次：1[WOS] [WOS记录] [WOS相关记录]
文献类型	期刊论文
条目标识符	https://kms.wmu.edu.cn/handle/3ETUA0LF/16446
专题	附属第一医院_儿科第一临床医学院（信息与工程学院）、附属第一医院第一临床医学院（信息与工程学院）、附属第一医院_浙江省胰脏肝脏危重性疾病重点实验室其他_附属第三医院（瑞安市人民医院）
通讯作者	Lu, Chao-Sheng; Wang, Hong-Wei
作者单位	1.The College of Medical Technology,Shanghai University of Medicine & Health Sciences,Shanghai,200000,China; 2.Department of Pediatrics,The First Affiliated Hospital of Wenzhou Medical University,322 Nanbaixiang Street,Wenzhou,325000,China; 3.The First Clinical Medical College of Wenzhou Medical University,Wenzhou,325000,China; 4.Ruian Center of Chinese-American Research Institute for Diabetic Complications,The Third Affiliated Hospital of Wenzhou Medical University,Wenzhou,325000,China; 5.Key Laboratory of Diagnosis and Treatment of Severe Hepato-Pancreatic Diseases of Zhejiang Province,The First Affiliated Hospital of Wenzhou Medical University,322 Nanbaixiang Street,Wenzhou,325000,China
通讯作者单位	附属第一医院; 第一临床医学院（信息与工程学院）、附属第一医院
推荐引用方式 GB/T 7714	Weng, Hua-Chun,Lu, Xin-Yu,Xu, Yu-Peng,et al. Fibroblast growth factor 21 attenuates salt-sensitive hypertension-induced nephropathy through anti-inflammation and anti-oxidation mechanism[J]. MOLECULAR MEDICINE,2021,27(1):147.
APA	Weng, Hua-Chun., Lu, Xin-Yu., Xu, Yu-Peng., Wang, Yi-Hong., Wang, Dan., ... & Wang, Hong-Wei. (2021). Fibroblast growth factor 21 attenuates salt-sensitive hypertension-induced nephropathy through anti-inflammation and anti-oxidation mechanism. MOLECULAR MEDICINE, 27(1), 147.
MLA	Weng, Hua-Chun,et al."Fibroblast growth factor 21 attenuates salt-sensitive hypertension-induced nephropathy through anti-inflammation and anti-oxidation mechanism".MOLECULAR MEDICINE 27.1(2021):147.