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研究生付艺研究论文被心血管权威期刊Hypertension接受
作者:  来源:   发布时间:2016-11-07 15:50:44  浏览次数:

Therapeutic potential of PGRN in hyperhomocysteinemia-induced cardiorenal dysfunction

 

Yi Fu1#, Yu Sun1#, Meng Zhou1, Xiaojie Wang1, Ziying Wang1, Xinbing Wei1, Yan Zhang1, Zeyu Su1, Kaili Liang1, Wei Tang2, and Fan Yi1*

 

1Department of Pharmacology, Shandong University School of Medicine, Jinan, China, 250012

2 Department of Biochemistry and Molecular Biology, Shandong University School of Medicine, Jinan, China, 250012

 

  

#Co-first authors, equally contributed to this work

 

Running title: Progranulin and homocysteine

 

*Send Correspondence and Reprint Requests to:  

Fan Yi, Ph.D
                   Department of Pharmacology

Shandong University School of Medicine

44#, Wenhua Xi Road,

                   Jinan, Shandong, 250012, P.R. China

Phone : 86-0531-88382616

Fax :   86-0531-88382616

E-mail: fanyi@sdu.edu.cn

 

Abstract

Hyperhomocysteinemia (hHcys) is an important independent risk factor for the development of cardiovascular disease (CVD) and end stage renal disease (ESRD). Although multiple approaches lowering the levels of homocysteine (Hcys) have been used in experimental studies and clinical trials, there is no effective therapy available to fully prevent Hcys-induced injury. Therefore, identifying key molecules in the pathogenic pathways may provide clues to develop new therapeutic strategies for the treatment of hHcys-associated injury beyond lowering the plasma Hcys levels. In this study, we found that the levels of progranulin (PGRN), an autocrine growth factor, were significantly reduced in the kidney and heart from a mouse model of hHcys. We further observed that in hHcys, PGRN-deficient mice significantly exacerbated cardiorenal injury as evidenced by higher levels of urinary albumin excretion, more severe renal morphological injuries including pronounced glomerular basement membrane (GBM) thickening and podocyte foot process effacement, and adverse myocardial remodeling versus wild type mice. Mechanistically, we found that PGRN-medicated Wnt/β-catenin signaling was one of the critical signal transduction pathways that links Hcys to cardiorenal injury. Importantly, we finally provided direct evidence for the therapeutic potential of PGRN in mice with hHcys by pretreatment with recombinant human PGRN (rPGRN). Collectively, our results suggest that PGRN may be an innovative therapeutic strategy for treating patients with hHcys.

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