Monitoring of patients with type 2 diabetes and nephropathy in a specialized diabetic nephropathy clinic seems to be beneficial

Stratigou, Theodora; Paikopoulou, Angeliki; Αποστολου, Θωμασ; Vlassopoulou, Barbara; Tsagarakis, Stelios; Ioannidis, G.

doi:10.1016/j.dsx.2018.04.012

Cited by 1 publication

(1 citation statement)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Diabetic nephropathy (DN) is a complication of diabetes mellitus (DM) that frequently results in renal disease [1]. Clinically, DN is characterized by a variety of symptoms such as albuminuria [2]. Many patients have progressive renal injury [3,4], despite the rapid development of therapies for DN [5][6][7].…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: XBP1 inhibits mesangial cell apoptosis in response to oxidative stress via the PTEN/AKT pathway in diabetic nephropathy

Wang

Qiu

et al. 2019

FEBS Open Bio

View full text Add to dashboard Cite

Diabetic nephropathy ( DN ) is a complication of diabetes mellitus ( DM ) that frequently results in renal disease, and is characterized by a variety of symptoms, including albuminuria. It has been shown that apoptosis of glomerular mesangial cells ( MC s) can aggravate albuminuria and contribute to the development of diabetic glomerulosclerosis. Hence, determination of the mechanisms leading to MC apoptosis may help us gain insights into the pathogenesis of DN . As our understanding of the role of high glucose ( HG ) in MC apoptosis remains elusive, we explored the interplay between X‐box binding protein 1 ( XBP 1) and MC apoptosis in this study. XBP 1 was observed to be downregulated both in vivo and in vitro . Treatment of XBP 1‐overexpressing cells with HG resulted in a decrease of reactive oxygen species ( ROS ) and a suppression of cell apoptosis, concomitant with decreases in cleaved caspase‐3 and Bax. Subsequent analyses demonstrated that XBP 1 overexpression inhibited the expression of phosphatase and tensin homolog deleted on chromosome ten ( PTEN ) and enhanced the activation of AKT in MC s exposed to HG . In addition, XBP 1‐induced injuries in MC were reversed by overexpression of PTEN , and XBP 1 inhibited apoptosis, which was mediated by the activated PTEN / AKT signaling pathway. Thus, our data indicate that XBP 1 can activate the PTEN / AKT signaling pathway, thereby alleviating oxidative stress caused by HG or MC apoptosis. These findings suggest that XBP 1 may have potential in the development of treatment methods for DN .

show abstract