scholarly journals Mechanisms of metabolic memory and renal hypoxia as a therapeutic target in diabetic kidney disease

2017 ◽  
Vol 8 (3) ◽  
pp. 261-271 ◽  
Author(s):  
Yosuke Hirakawa ◽  
Tetsuhiro Tanaka ◽  
Masaomi Nangaku
Keyword(s):  
Kidney Disease ◽  
Therapeutic Target ◽  
Diabetic Kidney Disease ◽  
Metabolic Memory ◽  
Diabetic Kidney

scholarly journals Connexin‐mediated cell communication in the kidney: A potential therapeutic target for future intervention of diabetic kidney disease?

2020 ◽  
Vol 105 (2) ◽  
pp. 219-229 ◽  
Author(s):  
Gareth W. Price ◽  
Joe A. Potter ◽  
Bethany M. Williams ◽  
Chelsy L. Cliff ◽  
Paul E. Squires ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Therapeutic Target ◽  
Diabetic Kidney Disease ◽  
Cell Communication ◽  
Potential Therapeutic Target ◽  
Diabetic Kidney

scholarly journals Interplay between RNA-binding protein HuR and Nox4 as a novel therapeutic target in diabetic kidney disease

2020 ◽  
Vol 36 ◽  
pp. 100968 ◽  
Author(s):  
Qian Shi ◽  
Doug-Yoon Lee ◽  
Denis Féliers ◽  
Hanna E. Abboud ◽  
Manzoor A. Bhat ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Therapeutic Target ◽  
Diabetic Kidney Disease ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Diabetic Kidney ◽  
Novel Therapeutic

scholarly journals Histone demethylase UTX is a therapeutic target for diabetic kidney disease

2018 ◽  
Vol 597 (6) ◽  
pp. 1643-1660 ◽  
Author(s):  
Hong Chen ◽  
Yixue Huang ◽  
Xiuqin Zhu ◽  
Chong Liu ◽  
Yangmian Yuan ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Therapeutic Target ◽  
Diabetic Kidney Disease ◽  
Histone Demethylase ◽  
Diabetic Kidney

scholarly journals Effects of metabolic memory on inflammation and fibrosis associated with diabetic kidney disease: an epigenetic perspective

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Wen Zheng ◽  
Jia Guo ◽  
Zhang-Suo Liu
Keyword(s):  
Kidney Disease ◽  
Environmental Factors ◽  
Diabetic Kidney Disease ◽  
Early Recognition ◽  
Epigenetic Modifications ◽  
Metabolic Memory ◽  
Diabetic Patients ◽  
Diabetic Kidney

AbstractDiabetic kidney disease (DKD) is one of the most common microvascular complication of both type 1 (T1DM) and type 2 diabetes mellitus (T2DM), and the leading cause of end-stage renal disease (ESRD) worldwide. Persistent inflammation and subsequent chronic fibrosis are major causes of loss of renal function, which is associated with the progression of DKD to ESRD. In fact, DKD progression is affected by a combination of genetic and environmental factors. Approximately, one-third of diabetic patients progress to develop DKD despite intensive glycemic control, which propose an essential concept “metabolic memory.” Epigenetic modifications, an extensively studied mechanism of metabolic memory, have been shown to contribute to the susceptibility to develop DKD. Epigenetic modifications also play a regulatory role in the interactions between the genes and the environmental factors. The epigenetic contributions to the processes of inflammation and fibrogenesis involved in DKD occur at different regulatory levels, including DNA methylation, histone modification and non-coding RNA modulation. Compared with genetic factors, epigenetics represents a new therapeutic frontier in understanding the development DKD and may lead to therapeutic breakthroughs due to the possibility to reverse these modifications therapeutically. Early recognition of epigenetic events and biomarkers is crucial for timely diagnosis and intervention of DKD, and for the prevention of the progression of DKD to ESRD. Herein, we will review the latest epigenetic mechanisms involved in the renal pathology of both type 1 (T1DN) and type 2 diabetic nephropathy (T2DN) and highlight the emerging role and possible therapeutic strategies based on the understanding of the role of epigenetics in DKD-associated inflammation and fibrogenesis.

Fumarate and TGF-P as Mediators of Metabolic Memory in Diabetic Kidney Disease

2015 ◽  
Vol 87 ◽  
pp. S26
Author(s):  
Antonio Anax Falcao de Oliveira ◽  
Larissa Leticia Bobadilla ◽  
Tiago Franco de Oliveira ◽  
Marisa Helena Gennari de Medeiros ◽  
Paolo Di Mascio ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Metabolic Memory ◽  
Diabetic Kidney

scholarly journals Role of Epigenetic Histone Modifications in Diabetic Kidney Disease Involving Renal Fibrosis

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Jing Sun ◽  
Yangwei Wang ◽  
Wenpeng Cui ◽  
Yan Lou ◽  
Guangdong Sun ◽  
...  
Keyword(s):  
Gene Expression ◽  
Kidney Disease ◽  
Histone Modifications ◽  
Renal Fibrosis ◽  
Diabetic Kidney Disease ◽  
Basement Membranes ◽  
Metabolic Memory ◽  
Diabetic Kidney ◽  
Mesenchymal Transition ◽  
Ecm Proteins

One of the commonest causes of end-stage renal disease is diabetic kidney disease (DKD). Renal fibrosis, characterized by the accumulation of extracellular matrix (ECM) proteins in glomerular basement membranes and the tubulointerstitium, is the final manifestation of DKD. The TGF-βpathway triggers epithelial-to-mesenchymal transition (EMT), which plays a key role in the accumulation of ECM proteins in DKD. DCCT/EDIC studies have shown that DKD often persists and progresses despite glycemic control in diabetes once DKD sets in due to prior exposure to hyperglycemia called “metabolic memory.” These imply that epigenetic factors modulate kidney gene expression. There is evidence to suggest that in diabetes and hyperglycemia, epigenetic histone modifications have a significant effect in modulating renal fibrotic and ECM gene expression induced by TGF-β1, as well as its downstream profibrotic genes. Histone modifications are also implicated in renal fibrosis through its ability to regulate the EMT process triggered by TGF-βsignaling. In view of this, efforts are being made to develop HAT, HDAC, and HMT inhibitors to delay, stop, or even reverse DKD. In this review, we outline the latest advances that are being made to regulate histone modifications involved in DKD.

scholarly journals Serotonin and Its Receptor as a New Antioxidant Therapeutic Target for Diabetic Kidney Disease

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Yu Yang ◽  
Hui Huang ◽  
Zheng Xu ◽  
Jun-kai Duan
Keyword(s):  
Oxidative Stress ◽  
Kidney Disease ◽  
Therapeutic Target ◽  
Diabetic Kidney Disease ◽  
Vascular Complications ◽  
Controlled Clinical Trials ◽  
Potential Therapeutic Target ◽  
Diabetic Kidney ◽  
Diabetic Vascular Complications ◽  
Physiological Pathways

Diabetic kidney disease (DKD) is a widespread chronic microvascular complication of diabetes mellitus (DM), affects almost 30–50% of patients, and represents a leading cause of death of DM. Serotonin or 5-hydroxytryptamine (5-HT) is a multifunctional bioamine that has crucial roles in many physiological pathways. Recently, emerging evidence from experimental and clinical studies has demonstrated that 5-HT is involved in the pathogenesis of diabetic vascular complications. The 5-HT receptor (5-HTR) antagonists exert renoprotective effects by suppressing oxidative stress, suggesting that 5-HTR can be used as a potential target for treating DKD. In this review, therefore, we summarize the published information available for the involvement of 5-HT and 5-HTR antagonists in the pathogenesis of various diabetic complications with a particular focus of DKD. We conclude that 5-HTR is a potential therapeutic target for treating DKD, as it has been successfully applied in animal models and has currently being investigated in randomized and controlled clinical trials.

Sign in / Sign up

Export Citation Format

Share Document