scholarly journals Reduced Krüppel-Like Factor 2 Aggravates Glomerular Endothelial Cell Injury and Kidney Disease in Mice with Unilateral Nephrectomy

2016 ◽  
Vol 186 (8) ◽  
pp. 2021-2031 ◽  
Author(s):  
Fang Zhong ◽  
Sandeep K. Mallipattu ◽  
Chelsea Estrada ◽  
Madhav Menon ◽  
Fadi Salem ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Kidney Disease ◽  
Cell Injury ◽  
Unilateral Nephrectomy ◽  
Glomerular Endothelial Cell ◽  
Endothelial Cell Injury

507-P: Changes of miR-223-3p May Play an Important Role in Renal Endothelial Cell Injury of Diabetes Kidney Disease (DKD)

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 507-P
Author(s):  
RONG LI ◽  
LIN JIE ◽  
JINGMEI LUO ◽  
ZHONGCE YANG ◽  
LIHUA ZHANG
Keyword(s):  
Endothelial Cell ◽  
Kidney Disease ◽  
Cell Injury ◽  
Endothelial Cell Injury

CD8+iTregs attenuate glomerular endothelial cell injury in lupus-prone mice through blocking the activation of p38 MAPK and NF-κB

2018 ◽  
Vol 103 ◽  
pp. 133-143 ◽  
Author(s):  
Ya Liu ◽  
Weijuan Deng ◽  
Qiaoyun Meng ◽  
Xiaonan Qiu ◽  
Dong Sun ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
P38 Mapk ◽  
Cell Injury ◽  
Glomerular Endothelial Cell ◽  
Endothelial Cell Injury

scholarly journals Glomerular endothelial cell injury and cross talk in diabetic kidney disease

2015 ◽  
Vol 308 (4) ◽  
pp. F287-F297 ◽  
Author(s):  
Jia Fu ◽  
Kyung Lee ◽  
Peter Y. Chuang ◽  
Zhihong Liu ◽  
John Cijiang He
Keyword(s):  
Endothelial Cell ◽  
Kidney Disease ◽  
Cross Talk ◽  
Diabetic Kidney Disease ◽  
Cell Injury ◽  
Mesangial Cells ◽  
Glomerular Endothelial Cell ◽  
Glomerular Cell ◽  
Diabetic Kidney ◽  
Endothelial Cell Surface

Diabetic kidney disease (DKD) remains a leading cause of new-onset end-stage renal disease (ESRD), and yet, at present, the treatment is still very limited. A better understanding of the pathogenesis of DKD is therefore necessary to develop more effective therapies. Increasing evidence suggests that glomerular endothelial cell (GEC) injury plays a major role in the development and progression of DKD. Alteration of the glomerular endothelial cell surface layer, including its major component, glycocalyx, is a leading cause of microalbuminuria observed in early DKD. Many studies suggest a presence of cross talk between glomerular cells, such as between GEC and mesangial cells or GEC and podocytes. PDGFB/PDGFRβ is a major mediator for GEC and mesangial cell cross talk, while vascular endothelial growth factor (VEGF), angiopoietins, and endothelin-1 are the major mediators for GEC and podocyte communication. In DKD, GEC injury may lead to podocyte damage, while podocyte loss further exacerbates GEC injury, forming a vicious cycle. Therefore, GEC injury may predispose to albuminuria in diabetes either directly or indirectly by communication with neighboring podocytes and mesangial cells via secreted mediators. Identification of novel mediators of glomerular cell cross talk, such as microRNAs, will lead to a better understanding of the pathogenesis of DKD. Targeting these mediators may be a novel approach to develop more effective therapy for DKD.

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