scholarly journals Targeting microRNAs as a Therapeutic Strategy to Reduce Oxidative Stress in Diabetes

2019 ◽  
Vol 20 (24) ◽  
pp. 6358 ◽  
Author(s):  
Giuseppina Emanuela Grieco ◽  
Noemi Brusco ◽  
Giada Licata ◽  
Laura Nigi ◽  
Caterina Formichi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Drug Delivery ◽  
Molecular Mechanisms ◽  
Cell Loss ◽  
Delivery Methods ◽  
Cell Dysfunction ◽  
Single Cell Type ◽  
Chronic Hyperglycaemia ◽  
Target Effects

Diabetes mellitus is a group of heterogeneous metabolic disorders characterized by chronic hyperglycaemia as a consequence of pancreatic β cell loss and/or dysfunction, also caused by oxidative stress. The molecular mechanisms involved inβ cell dysfunction and in response to oxidative stress are also regulated by microRNAs (miRNAs). miRNAs are a class of negative gene regulators, which modulate pathologic mechanisms occurring in diabetes and its complications. Although several pharmacological therapies specifically targeting miRNAs have already been developed and brought to the clinic, most previous miRNA-based drug delivery methods were unable to target a specific miRNA in a single cell type or tissue, leading to important off-target effects. In order to overcome these issues, aptamers and nanoparticles have been described as non-cytotoxic vehicles for miRNA-based drug delivery. These approaches could represent an innovative way to specifically target and modulate miRNAs involved in oxidative stress in diabetes and its complications. Therefore, the aims of this review are: (i) to report the role of miRNAs involved in oxidative stress in diabetes as promising therapeutic targets; (ii) to shed light onto the new delivery strategies developed to modulate the expression of miRNAs in diseases.

LncRNA SNHG12 Improves Cerebral Ischemic-reperfusion Injury by Activating SIRT1/FOXO3a Pathway through I nhibition of Autophagy and Oxidative Stress

2020 ◽  
Vol 17 (4) ◽  
pp. 394-401
Author(s):  
Yuanhua Wu ◽  
Yuan Huang ◽  
Jing Cai ◽  
Donglan Zhang ◽  
Shixi Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Cell Activity ◽  
Ht22 Cells ◽  
Cerebral Ischemic ◽  
Cerebral Ischemic Reperfusion ◽  
And Oxidative Stress

Background: Ischemia/reperfusion (I/R) injury involves complex biological processes and molecular mechanisms such as autophagy. Oxidative stress plays a critical role in the pathogenesis of I/R injury. LncRNAs are the regulatory factor of cerebral I/R injury. Methods: This study constructs cerebral I/R model to investigate role of autophagy and oxidative stress in cerebral I/R injury and the underline regulatory mechanism of SIRT1/ FOXO3a pathway. In this study, lncRNA SNHG12 and FOXO3a expression was up-regulated and SIRT1 expression was down-regulated in HT22 cells of I/R model. Results: Overexpression of lncRNA SNHG12 significantly increased the cell viability and inhibited cerebral ischemicreperfusion injury induced by I/Rthrough inhibition of autophagy. In addition, the transfected p-SIRT1 significantly suppressed the release of LDH and SOD compared with cells co-transfected with SIRT1 and FOXO3a group and cells induced by I/R and transfected with p-SNHG12 group and overexpression of cells co-transfected with SIRT1 and FOXO3 further decreased the I/R induced release of ROS and MDA. Conclusion: In conclusion, lncRNA SNHG12 increased cell activity and inhibited oxidative stress through inhibition of SIRT1/FOXO3a signaling-mediated autophagy in HT22 cells of I/R model. This study might provide new potential therapeutic targets for further investigating the mechanisms in cerebral I/R injury and provide.

scholarly journals Molecular Mechanisms of Obesity-Linked Cardiac Dysfunction: An Up-Date on Current Knowledge

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 629
Author(s):  
Jorge Gutiérrez-Cuevas ◽  
Ana Sandoval-Rodriguez ◽  
Alejandra Meza-Rios ◽  
Hugo Christian Monroy-Ramírez ◽  
Marina Galicia-Moreno ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Dysfunction ◽  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Peroxisome Proliferator ◽  
White Adipocyte ◽  
Peroxisome Proliferator Activated Receptors ◽  
And Oxidative Stress

Obesity is defined as excessive body fat accumulation, and worldwide obesity has nearly tripled since 1975. Excess of free fatty acids (FFAs) and triglycerides in obese individuals promote ectopic lipid accumulation in the liver, skeletal muscle tissue, and heart, among others, inducing insulin resistance, hypertension, metabolic syndrome, type 2 diabetes (T2D), atherosclerosis, and cardiovascular disease (CVD). These diseases are promoted by visceral white adipocyte tissue (WAT) dysfunction through an increase in pro-inflammatory adipokines, oxidative stress, activation of the renin-angiotensin-aldosterone system (RAAS), and adverse changes in the gut microbiome. In the heart, obesity and T2D induce changes in substrate utilization, tissue metabolism, oxidative stress, and inflammation, leading to myocardial fibrosis and ultimately cardiac dysfunction. Peroxisome proliferator-activated receptors (PPARs) are involved in the regulation of carbohydrate and lipid metabolism, also improve insulin sensitivity, triglyceride levels, inflammation, and oxidative stress. The purpose of this review is to provide an update on the molecular mechanisms involved in obesity-linked CVD pathophysiology, considering pro-inflammatory cytokines, adipokines, and hormones, as well as the role of oxidative stress, inflammation, and PPARs. In addition, cell lines and animal models, biomarkers, gut microbiota dysbiosis, epigenetic modifications, and current therapeutic treatments in CVD associated with obesity are outlined in this paper.

scholarly journals Role of Liposomes Composite as Drug Transport Mechanism

2021 ◽  
pp. 230-243
Keyword(s):  
Drug Delivery ◽  
Lipid Bilayers ◽  
Transport Mechanism ◽  
Drug Transport ◽  
Phospholipid Bilayer ◽  
Drug Transporter ◽  
Delivery Methods ◽  
Second Stage ◽  
Novel Drug

Liposomes are spherical shaped vesicles comprising of at least one phospholipid bilayer that serve as a novel drug delivery framework. They are microscopic structures in which a fluid system is totally encased by a film made out of lipid bilayers. It varies in size, conformation, charge and drug transporter stacked with assortment of particles, for example, small molecules of drug, plasmids, nucleotides or proteins and so on. Ongoing advances in nanotherapeutics have brought about engineered liposomes rising in nanomedicine, giving better restorative control of diseased states. This has made ready for the improvement of second-stage liposomes for increased efficiency and could at last lead to a change in perspective from the regular drug delivery methods.

scholarly journals Oxidative stress and ageing of the post-ovulatory oocyte

Reproduction ◽  
2013 ◽  
Vol 146 (6) ◽  
pp. R217-R227 ◽  
Author(s):  
Tessa Lord ◽  
R John Aitken
Keyword(s):  
Oxidative Stress ◽  
Molecular Mechanisms ◽  
Embryo Quality ◽  
Fertilization Rates ◽  
Molecular Events ◽  
Post Implantation ◽  
Potential Use

With extended periods of time following ovulation, the metaphase II stage oocyte experiences deterioration in quality referred to as post-ovulatory oocyte ageing. Post-ovulatory ageing occurs both in vivo and in vitro and has been associated with reduced fertilization rates, poor embryo quality, post-implantation errors and abnormalities in the offspring. Although the physiological consequences of post-ovulatory oocyte ageing have largely been established, the molecular mechanisms controlling this process are not well defined. This review analyses the relationships between biochemical changes exhibited by the ageing oocyte and the symptoms associated with the ageing phenotype. We also discuss molecular events that are potentially involved in orchestrating post-ovulatory ageing with a particular focus on the role of oxidative stress. We propose that oxidative stress may act as the initiator for a cascade of events that create the aged oocyte phenotype. Specifically, oxidative stress has the capacity to cause a decline in levels of critical cell cycle factors such as maturation-promoting factor, impair calcium homoeostasis, induce mitochondrial dysfunction and directly damage multiple intracellular components of the oocyte such as lipids, proteins and DNA. Finally, this review addresses current strategies for delaying post-ovulatory oocyte ageing with a particular focus on the potential use of compounds such as caffeine or selected antioxidants in the development of more refined media for the preservation of oocyte integrity during IVF procedures.

scholarly journals Biochemical Alterations in Semen of Varicocele Patients: A Review of the Literature

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Antonio Mancini ◽  
Roberto Festa ◽  
Sebastiano Raimondo ◽  
Andrea Silvestrini ◽  
Elena Giacchi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Surgical Treatment ◽  
Molecular Mechanisms ◽  
Coenzyme Q ◽  
Published Data ◽  
Sperm Cells ◽  
Review Of The Literature ◽  
Biochemical Alterations ◽  
Biochemical Abnormalities

Oxidative stress is a mechanism underlying different kinds of infertility in human males. However, different results can be observed in relation to the method used for its evaluation. Varicocele patients show a number of biochemical abnormalities, including an altered distribution of coenzyme Q between seminal plasma and sperm cells and also an apparent defect in the utilization of antioxidants. Moreover, an influence of systemic hormones on seminal antioxidant system was observed too. Finally, the effects of surgical treatment on oxidativestress indexes and the possible usefulness of some medical therapies, like coenzyme Q supplementation, are discussed. In conclusion, published data show a role of oxidative stress in varicocele-related male infertility, but at present we do not know the precise molecular mechanisms underlying these phenomena.

Natural Killer Cell Dysfunction in Uremia: The Role of Oxidative Stress and the Effects of Dialysis

2013 ◽  
Vol 35 (s2) ◽  
pp. 14-19 ◽  
Author(s):  
Marie-Noelle Peraldi ◽  
Jeannig Berrou ◽  
Fabien Métivier ◽  
Antoine Toubert
Keyword(s):  
Oxidative Stress ◽  
Natural Killer Cell ◽  
Natural Killer ◽  
Killer Cell ◽  
Cell Dysfunction

scholarly journals Molecular mechanisms of genetic damages of the myocardium in cardiomyopathy

2010 ◽  
Vol 56 (3) ◽  
pp. 319-328
Author(s):  
A.G. Hasanov ◽  
T.V. Bershova ◽  
E.N. Basargina ◽  
M.I. Bakanov
Keyword(s):  
Extracellular Matrix ◽  
Molecular Mechanisms ◽  
Genetic Factors ◽  
Cytoskeletal Proteins ◽  
Matrix Proteins ◽  
Force Generation ◽  
Cardiac Cell ◽  
Cell Dysfunction ◽  
Thick Filaments

The review highlighted problems of reorganization of myocardical contractile and cytoskeletal proteins in cardiomyopathy (CM). The role of the genetic factors coding contractile proteins, proteins of thin and thick filaments, and also extracellular matrix proteins in processes of formation and development of hypertrophic (HCM) and dilated (DCM) cardiomyopathy are analyzed. The mechanisms responsible for the changes in cardiac proteins on regulation involved into force generation, its transfer, recycling ATP, impairments in transmembranal signals, that finally lead to cardiac cell dysfunction determining various manifestations of CM are considered.

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