scholarly journals Insights into the Role of MicroRNAs in the Onset and Development of Diabetic Neuropathy

2019 ◽  
Vol 20 (18) ◽  
pp. 4627 ◽  
Author(s):  
Raffaele Simeoli ◽  
Alessandra Fierabracci
Keyword(s):  
Oxidative Stress ◽  
Diabetic Neuropathy ◽  
Peripheral Nerves ◽  
Recent Literature ◽  
Polyol Pathway ◽  
Cytokine Release ◽  
Chronic Hyperglycemia ◽  
Pathway Activation ◽  
Non Coding Rnas

Diabetic neuropathy is a serious complication of chronic hyperglycemia in diabetes patients. This complication can involve both peripheral sensorimotor and autonomic nervous system. The precise nature of injury to the peripheral nerves mediated by chronic hyperglycemia is unknown; however, several mechanisms have been proposed including polyol pathway activation, enhanced glycation of proteins and lipids, increased oxidative stress, and cytokine release in the site of injury. MicroRNAs (miRNAs) are small non-coding RNAs that mediate RNA interference by post-transcriptionally modulating gene expression and protein synthesis. Therefore, they have been implicated in several developmental, physiological, and pathophysiological processes where they modulate the expression of different proteins. Recently, miRNAs gained an increasing attention also for their role as diagnostic test in many diseases due to their stability in serum and their easy detection. Furthermore, recent studies suggest that miRNAs may be involved in diabetic neuropathy although their role in the onset and the development of this complication is not fully understood. In this review, we discuss the most recent literature providing evidence for miRNAs role in diabetic neuropathy opening new pathways to improve both early diagnosis and treatment of this complication.

scholarly journals Diabetic neuropathy: a focus on management

2020 ◽  
Vol 9 (1) ◽  
pp. 853-860
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Free Radicals ◽  
Glycemic Control ◽  
Diabetic Neuropathy ◽  
Peripheral Nerves ◽  
Metabolic Diseases ◽  
Polyol Pathway ◽  
Multiple Complication ◽  
Experience Pain

Diabetic neuropathy(DN) is a common troublesome ramification of diabetes mellitus impacting at least 50-60% patients of diabetes with multiple complication result in nerve damage, tingling, muscle wastage, sharp pains, burning and numbness in peripheral extremities more often experience pain in legs and feet. Hyperglycemia presents a central role in progression of DN that causes variations in the blood vessels providing blood to the peripheral nerves; metabolic diseases such as initiation of the polyol pathway, myo-inositol depletion, genetic deviations and elevated non-enzymatic glycation which causes the generation of free radicals or oxidative stress. Intense Glycemic control is vitalto the ultimate prevention of DN. Apart from allopathic treatments, there are various alternative treatments like herbal based therapies, acupuncture therapies and physiotherapies are used to improve pain and other symptoms of DN and its related complications. This review provides a summary of various therapies of DN for treatment and its management.

scholarly journals Neuroinflammation and Oxidative Stress in Diabetic Neuropathy: Futuristic Strategies Based on These Targets

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Reddemma Sandireddy ◽  
Veera Ganesh Yerra ◽  
Aparna Areti ◽  
Prashanth Komirishetty ◽  
Ashutosh Kumar
Keyword(s):  
Oxidative Stress ◽  
Diabetic Neuropathy ◽  
Nitrosative Stress ◽  
Microvascular Complications ◽  
Vascular Complications ◽  
Polyol Pathway ◽  
The Body ◽  
Nerve Tissue ◽  
Chronic Hyperglycemia ◽  
Hexosamine Pathway

In Diabetes, the chronic hyperglycemia and associated complications affecting peripheral nerves are one of the most commonly occurring microvascular complications with an overall prevalence of 50–60%. Among the vascular complications of diabetes, diabetic neuropathy is the most painful and disabling, fatal complication affecting the quality of life in patients. Several theories of etiologies surfaced down the lane, amongst which the oxidative stress mediated damage in neurons and surrounding glial cell has gained attention as one of the vital mechanisms in the pathogenesis of neuropathy. Mitochondria induced ROS and other oxidants are responsible for altering the balance between oxidants and innate antioxidant defence of the body. Oxidative-nitrosative stress not only activates the major pathways namely, polyol pathway flux, advanced glycation end products formation, activation of protein kinase C, and overactivity of the hexosamine pathway, but also initiates and amplifies neuroinflammation. The cross talk between oxidative stress and inflammation is due to the activation of NF-κB and AP-1 and inhibition of Nrf2, peroxynitrite mediate endothelial dysfunction, altered NO levels, and macrophage migration. These all culminate in the production of proinflammatory cytokines which are responsible for nerve tissue damage and debilitating neuropathies. This review focuses on the relationship between oxidative stress and neuroinflammation in the development and progression of diabetic neuropathy.

scholarly journals Long Non-coding RNA XIST Attenuates Diabetic Peripheral Neuropathy by Inducing Autophagy Through MicroRNA-30d-5p/sirtuin1 Axis

2021 ◽  
Vol 8 ◽  
Author(s):  
Bei-Yan Liu ◽  
Lin Li ◽  
Li-Wei Bai ◽  
Chang-Shui Xu
Keyword(s):  
Oxidative Stress ◽  
Peripheral Neuropathy ◽  
Schwann Cells ◽  
Diabetic Peripheral Neuropathy ◽  
Beclin 1 ◽  
Diabetic Mice ◽  
Non Coding Rna ◽  
Non Coding Rnas ◽  
Long Non Coding Rna

Diabetic peripheral neuropathy (DPN) is a prevalent diabetes mellitus (Feldman et al., 2017) complication and the primary reason for amputation. Meanwhile, long non-coding RNAs (lncRNAs) are a type of regulatory non-coding RNAs (ncRNAs) that broadly participate in DPN development. However, the correlation of lncRNA X-inactive specific transcript (XIST) with DPN remains unclear. In this study, we were interested in the role of XIST in the modulation of DPN progression. Significantly, our data showed that the expression of XIST and sirtuin1 (SIRT1) was inhibited, and the expression of microRNA-30d-5p (miR-30d-5p) was enhanced in the trigeminal sensory neurons of the diabetic mice compared with the normal mice. The levels of LC3II and Beclin-1 were inhibited in the diabetic mice. The treatment of high glucose (HG) reduced the XIST expression in Schwann cells. The apoptosis of Schwann cells was enhanced in the HG-treated cells, but the overexpression of XIST could block the effect in the cells. Moreover, the levels of LC3II and Beclin-1 were reduced in the HG-treated Schwann cells, while the overexpression of XIST was able to reverse this effect. The HG treatment promoted the production of oxidative stress, while the XIST overexpression could attenuate this result in the Schwann cells. Mechanically, XIST was able to sponge miR-30d-5p and miR-30d-5p-targeted SIRT1 in the Schwann cells. MiR-30d-5p inhibited autophagy and promoted oxidative stress in the HG-treated Schwann cells, and SIRT1 presented a reversed effect. MiR-30d-5p mimic or SIRT1 depletion could reverse XIST overexpression-mediated apoptosis and autophagy of the Schwann cells. Thus, we concluded that XIST attenuated DPN by inducing autophagy through miR-30d-5p/SIRT1 axis. XIST and miR-30d-5p may be applied as the potential targets for DPN therapy.

scholarly journals The Role of MicroRNAs in Diabetes-Related Oxidative Stress

2019 ◽  
Vol 20 (21) ◽  
pp. 5423 ◽  
Author(s):  
Mirza Muhammad Fahd Qadir ◽  
Dagmar Klein ◽  
Silvia Álvarez-Cubela ◽  
Juan Domínguez-Bendala ◽  
Ricardo Luis Pastori
Keyword(s):  
Oxidative Stress ◽  
Target Gene ◽  
Cellular Stress ◽  
Cellular Damage ◽  
Oxygen Species ◽  
Non Coding Rnas ◽  
And Oxidative Stress

Cellular stress, combined with dysfunctional, inadequate mitochondrial phosphorylation, produces an excessive amount of reactive oxygen species (ROS) and an increased level of ROS in cells, which leads to oxidation and subsequent cellular damage. Because of its cell damaging action, an association between anomalous ROS production and disease such as Type 1 (T1D) and Type 2 (T2D) diabetes, as well as their complications, has been well established. However, there is a lack of understanding about genome-driven responses to ROS-mediated cellular stress. Over the last decade, multiple studies have suggested a link between oxidative stress and microRNAs (miRNAs). The miRNAs are small non-coding RNAs that mostly suppress expression of the target gene by interaction with its 3’untranslated region (3′UTR). In this paper, we review the recent progress in the field, focusing on the association between miRNAs and oxidative stress during the progression of diabetes.

Damaging effects of hyperglycemia on cardiovascular function: spotlight on glucose metabolic pathways

2016 ◽  
Vol 310 (2) ◽  
pp. H153-H173 ◽  
Author(s):  
Rudo F. Mapanga ◽  
M. Faadiel Essop
Keyword(s):  
Oxidative Stress ◽  
Polyol Pathway ◽  
Cardiovascular Complications ◽  
Hexosamine Biosynthetic Pathway ◽  
Kinase C ◽  
Glycation End Products ◽  
Global Health Problem ◽  
Metabolic Cycle ◽  
Damaging Effects

The incidence of cardiovascular complications associated with hyperglycemia is a growing global health problem. This review discusses the link between hyperglycemia and cardiovascular diseases onset, focusing on the role of recently emerging downstream mediators, namely, oxidative stress and glucose metabolic pathway perturbations. The role of hyperglycemia-mediated activation of nonoxidative glucose pathways (NOGPs) [i.e., the polyol pathway, hexosamine biosynthetic pathway, advanced glycation end products (AGEs), and protein kinase C] in this process is extensively reviewed. The proposal is made that there is a unique interplay between NOGPs and a downstream convergence of detrimental effects that especially affect cardiac endothelial cells, thereby contributing to contractile dysfunction. In this process the AGE pathway emerges as a crucial mediator of hyperglycemia-mediated detrimental effects. In addition, a vicious metabolic cycle is established whereby hyperglycemia-induced NOGPs further fuel their own activation by generating even more oxidative stress, thereby exacerbating damaging effects on cardiac function. Thus NOGP inhibition, and particularly that of the AGE pathway, emerges as a novel therapeutic intervention for the treatment of cardiovascular complications such as acute myocardial infarction in the presence hyperglycemia.

Cadmium induced apoptosis in mouse primary hepatocytes: the role of oxidative stress-mediated ERK pathway activation and the involvement of histone H3 phosphorylation

RSC Advances ◽  
2015 ◽  
Vol 5 (40) ◽  
pp. 31798-31806 ◽  
Author(s):  
Jing Wang ◽  
Minglu Hao ◽  
Chunguang Liu ◽  
Rutao Liu
Keyword(s):  
Oxidative Stress ◽  
Histone H3 ◽  
Erk Signaling ◽  
Erk Pathway ◽  
Primary Hepatocytes ◽  
H3 Phosphorylation ◽  
Pathway Activation ◽  
Induced Apoptosis ◽  
Histone H3 Phosphorylation

Time-delayed apoptosis induced by cadmium in primary hepatocytes through DNA damage, histone modification and ERK signaling cascade, which are all mediated by oxidative stress.

scholarly journals LINC01158 works as an oncogene in glioma via sponging miR-6734-3p to boost CENPK expression

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Zhenxing Sun ◽  
Naili Wei ◽  
Shenglian Yao ◽  
Guihuai Wang ◽  
Yaxing Sun ◽  
...  
Keyword(s):  
Glioma Cell ◽  
Caspase 3 ◽  
Recent Literature ◽  
Subcellular Fractionation ◽  
Luciferase Reporter ◽  
Biological Functions ◽  
Positive Regulation ◽  
Qrt Pcr ◽  
Non Coding Rnas

Abstract Background Long non-coding RNAs (lncRNAs) have been certified to play vital biological functions in glioma and have received considerable attention in the recent literature. Nonetheless, the role of LINC01158 in glioma remains to be elucidated. Methods qRT-PCR, western blot and GEPIA database were applied for reporting the expression of CENPK and LINC01158 in glioma and the correlation between LINC01158 and CENPK expression. EdU, colony formation, CCK-8, caspase-3 activity and TUNEL assays probed the impacts of LINC01158 on glioma cell growth. Subcellular fractionation and FISH assays revealed the cellular distribution of LINC01158. Luciferase reporter and RIP assays examined ceRNA network of LINC01158, CENPK and miR-6734-3p. Results LINC01158 and CENPK were both overexpressed in glioma and a positive regulation of LINC01158 on CENPK was corroborated. LINC01158 served a pro-proliferative and anti-apoptotic part in glioma by sponging miR-6734-3p to augment CENPK. Conclusion LINC01158 enhances CENPK by serving as sponge for miR-6734-3p to facilitate glioma development, proposing LINC01158 as a new player in glioma.

Sign in / Sign up

Export Citation Format

Share Document