scholarly journals Possible Relationship between Adiponectin and Renal Tubular Injury in Diabetic Nephropathy

2006 ◽  
Vol 53 (6) ◽  
pp. 745-752 ◽  
Author(s):  
Hiroki FUJITA ◽  
Tsukasa MORII ◽  
Jun KOSHIMURA ◽  
Motoko ISHIKAWA ◽  
Masako KATO ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Tubular Injury ◽  
Renal Tubular

scholarly journals Rap1 Ameliorates Renal Tubular Injury in Diabetic Nephropathy

Diabetes ◽  
2013 ◽  
Vol 63 (4) ◽  
pp. 1366-1380 ◽  
Author(s):  
L. Xiao ◽  
X. Zhu ◽  
S. Yang ◽  
F. Liu ◽  
Z. Zhou ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Tubular Injury ◽  
Renal Tubular

scholarly journals Study on Association of Pentraxin 3 and Diabetic Nephropathy in a Rat Model

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Xuehai Chen ◽  
Jiao Luo ◽  
Minmin Wu ◽  
Zhuo Pan ◽  
Yue Xie ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Islet Transplantation ◽  
Renal Injury ◽  
Microvascular Disease ◽  
Renal Tissue ◽  
Diabetic Rats ◽  
Diabetic Patients ◽  
Tubular Injury ◽  
Clinical Progression ◽  
Renal Tubular

Diabetic nephropathy (DN) is a serious microvascular complication of diabetes. Compared with other therapies for diabetic patients, islet transplantation can effectively prevent and reverse diabetes-induced microvascular disease, such as diabetic retinopathy and nephropathy. PTX3 is the only long pentraxin that can be detected in renal tissue. In this study, we investigated the expression of PTX3 when early DN was reversed after islet transplantation.Methods. Diabetes was induced in rats by injecting streptozotocin (STZ). Twelve weeks later, the diabetic rats were divided into 2 groups: the islet transplantation group (IT) and the diabetic nephropathy group (DN). Renal injury, renal function, and the expression of PTX3 in the plasma and the kidneys were assessed with urinalysis, immunohistochemical staining, and Western blot, respectively.Results. The expression of PTX3 in the kidney was significantly decreased in the DN group but increased in the IT group because of the reversal of DN.Conclusions. Our data showed that the level of PTX3 in renal tissue is closely related to renal injury in DN. This may be used to quantify the extent of renal injury in DN, provide a potential early indicator of renal tubular injury in early DN patients, and assess DN clinical progression.

scholarly journals Renal tubular ACE-mediated tubular injury is the major contributor to microalbuminuria in early diabetic nephropathy

2018 ◽  
Vol 314 (4) ◽  
pp. F531-F542 ◽  
Author(s):  
Masahiro Eriguchi ◽  
Mercury Lin ◽  
Michifumi Yamashita ◽  
Tuantuan V. Zhao ◽  
Zakir Khan ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Developed Countries ◽  
Tubular Injury ◽  
Wild Type ◽  
Tubulointerstitial Injury ◽  
Renal Tubular ◽  
Early Diabetic Nephropathy

Diabetic nephropathy is a major cause of end-stage renal disease in developed countries. While angiotensin-converting enzyme (ACE) inhibitors are used to treat diabetic nephropathy, how intrarenal ACE contributes to diabetic renal injury is uncertain. Here, two mouse models with different patterns of renal ACE expression were studied to determine the specific contribution of tubular vs. glomerular ACE to early diabetic nephropathy: it-ACE mice, which make endothelial ACE but lack ACE expression by renal tubular epithelium, and ACE 3/9 mice, which lack endothelial ACE and only express renal ACE in tubular epithelial cells. The absence of endothelial ACE normalized the glomerular filtration rate and endothelial injury in diabetic ACE 3/9 mice. However, these mice developed tubular injury and albuminuria and displayed low renal levels of megalin that were similar to those observed in diabetic wild-type mice. In diabetic it-ACE mice, despite hyperfiltration, the absence of renal tubular ACE greatly reduced tubulointerstitial injury and albuminuria and increased renal megalin expression compared with diabetic wild-type and diabetic ACE 3/9 mice. These findings demonstrate that endothelial ACE is a central regulator of the glomerular filtration rate while tubular ACE is a key player in the development of tubular injury and albuminuria. These data suggest that tubular injury, rather than hyperfiltration, is the main cause of microalbuminuria in early diabetic nephropathy.

scholarly journals Atrasentan increased the expression of klotho by mediating miR-199b-5p and prevented renal tubular injury in diabetic nephropathy

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Wen-Ling Kang ◽  
Gao-Si Xu
Keyword(s):  
Diabetic Nephropathy ◽  
High Glucose ◽  
Tubular Injury ◽  
Mice Model ◽  
Renal Tubular Cells ◽  
Proximal Tubular ◽  
Renal Proximal Tubular ◽  
Renal Tubular

Abstract Atrasentan is a promising therapy for treating diabetic nephropathy (DN). Here we evaluated whether atrasentan down-regulated the miR-199b-5p expression, thereby increasing klotho and preventing renal tubular injury in DN. One-hundred patients with type 2 diabetes mellitus (T2DM) and 40 healthy subjects were included. A DN mice model was established by an injection of streptozotocin (STZ). Human renal proximal tubular epithelial HK-2 cells were exposed to high glucose (20 mmol/L). Treated the mice and HK-2 cells with atrasentan and we then investigated whether and how miR-199b-5p and Klotho were involved in preventing renal tubular injury in DN. In patients, the serum miR-199b-5p level increased and the klotho concentration decreased in accordance with elevated albuminuria. Atrasentan down-regulated miR-199b-5p and up-regulated klotho of the DN mice and HK-2 cells exposed to high glucose. High glucose promoted the binding of histone H3 to the miR-199b-5p promoter and atrasentan canceled this effect. MiR-199b-5p targeted the 3′ UTR of klotho. Overexpression of miR-199b-5p canceled the effects of atrasentan on klotho expression and apoptosis of renal tubular cells in both in vivo and in vitro. The increased serum klotho, mediated by miR-199b-5p, is a possible mechanism by which atrasentan prevents renal tubular injury in DN.

470-P: SIK2 Protects against Renal Tubular Injury by Inhibiting Endoplasmic Reticulum Stress

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 470-P
Author(s):  
XIAOYU LIAO ◽  
BINGYAO LIU ◽  
HONGTING ZHENG
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Tubular Injury ◽  
Renal Tubular
Sign in / Sign up

Export Citation Format

Share Document