scholarly journals Mesenchymal Stem Cell Therapy in Diabetic Cardiomyopathy

Cells ◽  
2022 ◽  
Vol 11 (2) ◽  
pp. 240
Author(s):  
Jaqueline S. da Silva ◽  
Renata G. J. Gonçalves ◽  
Juliana F. Vasques ◽  
Bruna S. Rocha ◽  
Bianca Nascimento-Carlos ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Cardiac Remodeling ◽  
Cardiac Dysfunction ◽  
Conventional Treatment ◽  
Cardiovascular Complications ◽  
Cardiac Complications ◽  
Inflammatory Condition ◽  
Mesenchymal Stem Cell Therapy ◽  
Prevalence Of Diabetes Mellitus

The incidence and prevalence of diabetes mellitus (DM) are increasing worldwide, and the resulting cardiac complications are the leading cause of death. Among these complications is diabetes-induced cardiomyopathy (DCM), which is the consequence of a pro-inflammatory condition, oxidative stress and fibrosis caused by hyperglycemia. Cardiac remodeling will lead to an imbalance in cell survival and death, which can promote cardiac dysfunction. Since the conventional treatment of DM generally does not address the prevention of cardiac remodeling, it is important to develop new alternatives for the treatment of cardiovascular complications induced by DM. Thus, therapy with mesenchymal stem cells has been shown to be a promising approach for the prevention of DCM because of their anti-apoptotic, anti-fibrotic and anti-inflammatory effects, which could improve cardiac function in patients with DM.

scholarly journals Oxidative Stress as A Mechanism for Functional Alterations in Cardiac Hypertrophy and Heart Failure

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 931
Author(s):  
Anureet K. Shah ◽  
Sukhwinder K. Bhullar ◽  
Vijayan Elimban ◽  
Naranjan S. Dhalla
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Angiotensin Ii ◽  
Cardiac Hypertrophy ◽  
Cardiac Remodeling ◽  
Cardiac Dysfunction ◽  
Critical Role ◽  
Pressure Overload ◽  
Hypertrophied Heart ◽  
Vasoactive Hormones

Although heart failure due to a wide variety of pathological stimuli including myocardial infarction, pressure overload and volume overload is associated with cardiac hypertrophy, the exact reasons for the transition of cardiac hypertrophy to heart failure are not well defined. Since circulating levels of several vasoactive hormones including catecholamines, angiotensin II, and endothelins are elevated under pathological conditions, it has been suggested that these vasoactive hormones may be involved in the development of both cardiac hypertrophy and heart failure. At initial stages of pathological stimuli, these hormones induce an increase in ventricular wall tension by acting through their respective receptor-mediated signal transduction systems and result in the development of cardiac hypertrophy. Some oxyradicals formed at initial stages are also involved in the redox-dependent activation of the hypertrophic process but these are rapidly removed by increased content of antioxidants in hypertrophied heart. In fact, cardiac hypertrophy is considered to be an adaptive process as it exhibits either normal or augmented cardiac function for maintaining cardiovascular homeostasis. However, exposure of a hypertrophied heart to elevated levels of circulating hormones due to pathological stimuli over a prolonged period results in cardiac dysfunction and development of heart failure involving a complex set of mechanisms. It has been demonstrated that different cardiovascular abnormalities such as functional hypoxia, metabolic derangements, uncoupling of mitochondrial electron transport, and inflammation produce oxidative stress in the hypertrophied failing hearts. In addition, oxidation of catecholamines by monoamine oxidase as well as NADPH oxidase activation by angiotensin II and endothelin promote the generation of oxidative stress during the prolonged period by these pathological stimuli. It is noteworthy that oxidative stress is known to activate metallomatrix proteases and degrade the extracellular matrix proteins for the induction of cardiac remodeling and heart dysfunction. Furthermore, oxidative stress has been shown to induce subcellular remodeling and Ca2+-handling abnormalities as well as loss of cardiomyocytes due to the development of apoptosis, necrosis, and fibrosis. These observations support the view that a low amount of oxyradical formation for a brief period may activate redox-sensitive mechanisms, which are associated with the development of cardiac hypertrophy. On the other hand, high levels of oxyradicals over a prolonged period may induce oxidative stress and cause Ca2+-handling defects as well as protease activation and thus play a critical role in the development of adverse cardiac remodeling and cardiac dysfunction as well as progression of heart failure.

scholarly journals Endothelial Dysfunction in Diabetes Mellitus: Possible Involvement of Endoplasmic Reticulum Stress?

2012 ◽  
Vol 2012 ◽  
pp. 1-14 ◽  
Author(s):  
Basma Basha ◽  
Samson Mathews Samuel ◽  
Chris R. Triggle ◽  
Hong Ding
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Clinical Trials ◽  
Endoplasmic Reticulum ◽  
Endothelial Dysfunction ◽  
Er Stress ◽  
Vascular Complications ◽  
Cardiovascular Complications ◽  
Therapeutic Agents ◽  
Recent Past

The vascular complications of diabetes mellitus impose a huge burden on the management of this disease. The higher incidence of cardiovascular complications and the unfavorable prognosis among diabetic individuals who develop such complications have been correlated to the hyperglycemia-induced oxidative stress and associated endothelial dysfunction. Although antioxidants may be considered as effective therapeutic agents to relieve oxidative stress and protect the endothelium, recent clinical trials involving these agents have shown limited therapeutic efficacy in this regard. In the recent past experimental evidence suggest that endoplasmic reticulum (ER) stress in the endothelial cells might be an important contributor to diabetes-related vascular complications. The current paper contemplates the possibility of the involvement of ER stress in endothelial dysfunction and diabetes-associated vascular complications.

scholarly journals Glutathione “Redox Homeostasis” and Its Relation to Cardiovascular Disease

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Vladan P. Bajic ◽  
Christophe Van Neste ◽  
Milan Obradovic ◽  
Sonja Zafirovic ◽  
Djordje Radak ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Dysfunction ◽  
Redox Homeostasis ◽  
Cardiovascular Complications ◽  
Homeostatic Mechanism ◽  
Redox Mechanism ◽  
Signaling Mechanisms ◽  
Research Findings ◽  
Glutathione Redox

More people die from cardiovascular diseases (CVD) than from any other cause. Cardiovascular complications are thought to arise from enhanced levels of free radicals causing impaired “redox homeostasis,” which represents the interplay between oxidative stress (OS) and reductive stress (RS). In this review, we compile several experimental research findings that show sustained shifts towards OS will alter the homeostatic redox mechanism to cause cardiovascular complications, as well as findings that show a prolonged antioxidant state or RS can similarly lead to such cardiovascular complications. This experimental evidence is specifically focused on the role of glutathione, the most abundant antioxidant in the heart, in a redox homeostatic mechanism that has been shifted towards OS or RS. This may lead to impairment of cellular signaling mechanisms and elevated pools of proteotoxicity associated with cardiac dysfunction.

scholarly journals Diabetes mellitus activates fetal gene program and intensifies cardiac remodeling and oxidative stress in aged spontaneously hypertensive rats

2013 ◽  
Vol 12 (1) ◽  
pp. 152 ◽  
Author(s):  
Camila Rosa ◽  
Natasha Xavier ◽  
Dijon Henrique Campos ◽  
Ana Angélica Fernandes ◽  
Marcelo Diarcadia Cezar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Cardiac Remodeling ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
And Oxidative Stress

scholarly journals Evolution of Inflammatory and Oxidative Stress Markers in Romanian Obese Male Patients with Type 2 Diabetes Mellitus after Laparoscopic Sleeve Gastrectomy: One Year Follow-Up

Metabolites ◽  
2020 ◽  
Vol 10 (8) ◽  
pp. 308
Author(s):  
Ariana Picu ◽  
Laura Petcu ◽  
Diana Simona Ştefan ◽  
Grațiela Grădișteanu Pîrcălăbioru ◽  
Manuela Mitu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Sleeve Gastrectomy ◽  
Visceral Fat ◽  
Conventional Treatment ◽  
Male Patients ◽  
Obese Male

Geography is one of the key drivers of the significant variation in the etiopathogenic profile and prevalence of type 2 diabetes mellitus (T2DM) and obesity, therefore geographically based data are fundamental for implementing the appropriate interventions. Presently, the selection criteria of T2DM and obesity patients for laparoscopic sleeve gastrectomy (LSG) have not reached a worldwide consensus—highlighting the need for sharing experts’ guidance in the preoperative evaluation, choice of the interventional procedure, perioperative management and patient long-term care. The aim of the current study was to evaluate the impact of LSG on T2DM (T2DM) remission in Romanian obese male patients, based on a multiparametric, prospective investigation. We have conducted a randomized controlled study on 41 obese male participants with the body mass index (BMI) ≥ 30 kg/m2, aged 30–65 years, which were randomly divided in two study groups: one receiving conventional treatment and the second undergoing LSG. The clinical and anthropometrical parameters, resting metabolic rate, general biochemical status, adipocytes profile, gastrointestinal hormones levels, proinflammatory, oxidant and antioxidant profiles were determined at three time points: V1 (baseline), V2 (after six months) and V3 (after 12 months). Glycated hemoglobin (HbA1c), blood glucose levels, BMI, weight, visceral fat level, HDL-cholesterol, incretin hormones, proinflammatory and the oxidative stress status were significantly improved in the LSG versus conventional treatment group. This is the first study reporting on the evaluation of metabolic surgery impact on Romanian obese male patients with T2DM. Our results confirm that LSG could contribute to T2DM remission in patients with diabesity, but this beneficial effect seems to be critically influenced by the duration of T2DM rather than by the obesity status. Our results show that, in addition to the parameters included in the prediction algorithm, the proinsulin levels, proinsulin/insulin ratio and the visceral fat percentage could bring added value to the assessment of metabolic status.

scholarly journals Hypertension and diabetes mellitus association to oxidative stress in an elderly population

2018 ◽  
Author(s):  
Aleida Rodríguez-Castañenda ◽  
Katia Leticia Martínez-Gonzáles ◽  
Rosalinda Sánchez-Arenas ◽  
Sergio Sánchez-García ◽  
Israel Grijalva ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Elderly Population ◽  
Influential Factor ◽  
Control Group ◽  
Oxygen Species ◽  
Group 12 ◽  
High Prevalence ◽  
Prevalence Of Diabetes Mellitus

AbstractBackgroundMexico City has the highest aging rate in the country, as well as a high prevalence of diabetes mellitus (DM) and arterial hypertension (HT). All three on their own, are known to increase oxidative stress (OE).MethodsFinal groups included 18 patients without DM or HT (control group), 12 with DM, 23 with HT, and 18 with DM and HT. The EO was measured by the quantification of reactive oxygen species (ROS), and by determination of lipid peroxidation.ResultsHAS patients showed increased ROS levels as did men with HAS compared with the respective DM and HT groups. Also, women of the control group showed higher levels of ROS compared with men. HT in an aged population turned out to be the most influential factor for oxidative stress increase while DM had no effect whatsoever.

scholarly journals Frequency of Cardiovascular Complications and Its Association with Prognosis of COVID-19 Patients

2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Hossein Mazaherpour ◽  
Masoumeh Soofian ◽  
Elham Farahani ◽  
Fatemeh Masfari Farahani ◽  
Ehsanollah Ghaznavi Rad ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Troponin I ◽  
Cardiovascular Complications ◽  
Cardiac Complications ◽  
Age Difference ◽  
Creatine Kinase Mb ◽  
Significant Difference ◽  
Artery Disease ◽  
Underlying Diseases ◽  
Electrocardiogram Ecg

Coronavirus disease 2019 (COVID-19) may lead to acute respiratory disease; cardiovascular, gastrointestinal, and coagulation complications; and even death. One of the major complications is cardiovascular disorders, including arrhythmias, myocarditis, pericarditis, and acute coronary artery disease. The aim of this study was to evaluate the frequency of cardiovascular complications and to determine its association with the prognosis of COVID-19 patients. In a prospective analytic study, 137 hospitalized COVID-19 patients were enrolled. During hospitalization, an electrocardiogram (ECG) was performed every other day, and laboratory tests such as cardiac troponin I (cTnI) and creatine kinase-MB (CK-MB) were done 0, 6, and 12 hours after admission. These tests were repeated for patients with chest pain or ECG changes. Patients were categorized into three groups (improved, complicated, and expired patients) and assessed for the rate and type of arrhythmias, cardiac complications, lab tests, and outcomes of treatments. There was no significant relationship among the three groups related to primary arrhythmia and arrhythmias during treatment. The most common arrhythmia during hospitalization and after treatment was ST-T fragment changes. There was a significant age difference between the three groups ( P = 0.001 ). There was a significant difference among the three groups for some underlying diseases, including diabetes mellitus ( P = 0.003 ) and hyperlipidemia ( P = 0.004 ). In our study, different types of arrhythmias had no association with patients’ outcomes but age over 60 years, diabetes mellitus, and hyperlipidemia played an important role in the prognosis of COVID-19 cases.

scholarly journals Hyperglycemia Induces Myocardial Dysfunction via Epigenetic Regulation of JunD

2020 ◽  
Vol 127 (10) ◽  
pp. 1261-1273
Author(s):  
Shafaat Hussain ◽  
Abdul Waheed Khan ◽  
Alexander Akhmedov ◽  
Rosa Suades ◽  
Sarah Costantino ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Reactive Oxygen Species ◽  
Protein Expression ◽  
Cardiac Dysfunction ◽  
Nicotinamide Adenine Dinucleotide ◽  
Myocardial Dysfunction ◽  
Left Ventricular ◽  
Oxygen Species ◽  
Mrna And Protein Expression

Rationale: Hyperglycemia -induced reactive oxygen species are key mediators of cardiac dysfunction. JunD (Jund proto-oncogene subunit), a member of the AP-1 (activator protein-1) family of transcription factors, is emerging as a major gatekeeper against oxidative stress. However, its contribution to redox state and inflammation in the diabetic heart remains to be elucidated. Objective: The present study investigates the role of JunD in hyperglycemia-induced and reactive oxygen species–driven myocardial dysfunction. Methods and Results: JunD mRNA and protein expression were reduced in the myocardium of mice with streptozotocin-induced diabetes mellitus as compared to controls. JunD downregulation was associated with oxidative stress and left ventricular dysfunction assessed by electron spin resonance spectroscopy as well as conventional and 2-dimensional speckle-tracking echocardiography. Furthermore, myocardial expression of free radical scavenger superoxide dismutase 1 and aldehyde dehydrogenase 2 was reduced, whereas the NOX2 (NADPH [nicotinamide adenine dinucleotide phosphatase] oxidase subunit 2) and NOX4 (NADPH [nicotinamide adenine dinucleotide phosphatase] oxidase subunit 4) were upregulated. The redox changes were associated with increased NF-κB (nuclear factor kappa B) binding activity and expression of inflammatory mediators. Interestingly, mice with cardiac-specific overexpression of JunD via the α MHC (α- myosin heavy chain) promoter (α MHC JunD tg ) were protected against hyperglycemia-induced cardiac dysfunction. We also showed that JunD was epigenetically regulated by promoter hypermethylation, post-translational modification of histone marks, and translational repression by miRNA (microRNA)-673/menin. Reduced JunD mRNA and protein expression were confirmed in left ventricular specimens obtained from patients with type 2 diabetes mellitus as compared to nondiabetic subjects. Conclusions: Here, we show that a complex epigenetic machinery involving DNA methylation, histone modifications, and microRNAs mediates hyperglycemia-induced JunD downregulation and myocardial dysfunction in experimental and human diabetes mellitus. Our results pave the way for tissue-specific therapeutic modulation of JunD to prevent diabetic cardiomyopathy.

Kalpaamruthaa ameliorates myocardial and aortic damage in cardiovascular complications associated with type 2 diabetes mellitus

2013 ◽  
Vol 91 (2) ◽  
pp. 116-123 ◽  
Author(s):  
Raja Latha ◽  
Palanivelu Shanthi ◽  
Panchanadham Sachdanandam
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Body Mass ◽  
Protective Efficacy ◽  
Cardiovascular Complications ◽  
Matrix Metalloproteinase 2 ◽  
Ultrastructural Changes

Myocardial and aortic damage in cardiovascular complications (CVD) associated with type 2 diabetes mellitus and the protective efficacy of Kalpaamruthaa (KA) are evaluated in this study. CVD developed in 8 weeks after type 2 diabetes mellitus was induced by the administration of a high-fat diet for 2 weeks, and then with streptozotocin (2 × 35 mg·(kg body mass)–1, by intraperitonal injection, at 24 h intervals) in male Sprague–Dawley rats. CVD-induced rats were treated with KA at 200 mg·(kg body mass)–1·(day)–1 orally for 28 days. Increased oxidative stress in CVD-induced rats lowers antioxidant defense in the aorta. Treatment with KA reduced oxidative stress by increasing antioxidant status with decreased lipid peroxides in CVD-induced rats. Histological examination of the myocardium and aorta provided support for the cytoprotective effect of KA in CVD. Ultrastructural changes in the myocardium of CVD-induced rats were improved by KA treatment. Aortic damage was observed through decreased endothelial nitric oxide synthase and increased NADPH oxidase mRNA expressions in CVD-induced rats. KA reduced the aortic damage by ameliorating these levels back to normal. KA treatment reduced the pro-inflammatory cytokines tumor necrosis factor-α and interleukin 6 in CVD-induced rats. Immunohistochemical expressions of matrix metalloproteinase-2 and -9 were observed to be elevated in the myocardium of CVD-induced rats, but these were decreased by the administration of KA. This study demonstrates the cardiovascular protective effect of KA in type 2 diabetes.

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