Iron-Induced Damage in Cardiomyopathy: Oxidative-Dependent and Independent Mechanisms

Gammella, Elena; Recalcati, Stefania; Rybińska, Ilona; Buratti, Paolo; Cairo, Gaetano

doi:10.1155/2015/230182

Cited by 131 publications

(92 citation statements)

References 95 publications

(119 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These events enhance the destructions in insulin signaling, diminished endothelialmediated vaso-relaxation and associated renal and cardiovascular risks [12]. Similarly, acute hypoxia in the body is accumulating extracellular and cytosolic irons that damage the cardiovascular tissue which is also a reason of redox homeostatic imbalance that leads to hypertension and progression of metabolic dysregulation [13].…”

Section: Metabolic Syndrome and Mitochondrial Dysfunction: A Complex mentioning

confidence: 99%

Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

Jha

Kumar

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

View full text Add to dashboard Cite

Mounting evidence suggests a link between metabolic syndrome (MetS) such as diabetes, obesity, non-alcoholic fatty liver disease in the progression of Alzheimer's disease (AD), Parkinson's disease (PD) and other neurodegenerative diseases (NDDs). For instance, accumulated Aβ oligomer is enhancing neuronal Ca release and neural NO where increased NO level in the brain through post translational modification is modulating the level of insulin production. It has been further confirmed that irrespective of origin; brain insulin resistance triggers a cascade of the neurodegeneration phenomenon which can be aggravated by free reactive oxygen species burden, ER stress, metabolic dysfunction, neuorinflammation, reduced cell survival and altered lipid metabolism. Moreover, several studies confirmed that MetS and diabetic sharing common mechanisms in the progression of AD and NDDs where mitochondrial dynamics playing a critical role. Any mutation in mitochondrial DNA, exposure of environmental toxin, high-calorie intake, homeostasis imbalance, glucolipotoxicity is causative factors for mitochondrial dysfunction. These cumulative pleiotropic burdens in mitochondria leads to insulin resistance, increased ROS production; enhanced stress-related enzymes that is directly linked MetS and diabetes in neurodegeneration. Since, the linkup mechanism between mitochondrial dysfunction and disease phenomenon of both MetS and NDDs is quite intriguing, therefore, it is pertinent for the researchers to identify and implement the therapeutic interventions for targeting MetS and NDDs. Herein, we elucidated the pertinent role of MetS induced mitochondrial dysfunction in neurons and their consequences in NDDs. Further, therapeutic potential of well-known biomolecules and chaperones to target altered mitochondria has been comprehensively documented. This article is part of a Special Issue entitled: Oxidative Stress and Mitochondrial Quality in Diabetes/Obesity and Critical Illness Spectrum of Diseases - edited by P. Hemachandra Reddy.

show abstract

Section: Metabolic Syndrome and Mitochondrial Dysfunction: A Complex mentioning

confidence: 99%

Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

Jha

Kumar

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

View full text Add to dashboard Cite

show abstract

“…All the cell types that constitute the heart may be susceptible to ROS-induced damage, including endothelial cells and the cardiomyocytes. Iron's toxicity within cells arises from its capacity to catalyse the production of ROS that cause lipid peroxidation and organelle damage, which leads to cell death and fibrosis and ultimately impaired systolic and diastolic function [49] [50].…”

Section: Discussionmentioning

confidence: 99%

Alterations in Low-Z Elements Distribution in Heart Tissue after Treatments to Breast Cancer Using LEXRF Technique

Mantuano¹,

Barroso²,

Nogueira³

et al. 2016

AJAC

View full text Add to dashboard Cite

Data from Global Cancer Statistics show that breast cancer (BC) is the most common type of cancer among women, leading the number of deaths caused by cancer. The developments in diagnosis and treatment techniques for the BC, including chemotherapy and/or radiotherapy, increased the survival rates for this type of cancer. One late complication induced by BC treatment is the cardiotoxicity. This term comprises different cardiotoxic side effects, which include blood pressure alterations, myocardial ischemia, congestive heart failure and other damages. This study aimed to evaluate the cardiac alterations induced by radiotherapy and chemotherapy, simulating a treatment for BC in Wistar rats. It is, therefore, important to understand the mechanisms involved in the cardiotoxicity, in order to prevent women from this late effect, when they undergo BC treatments. The major interests in this work are in Low atomic weight elements as Sodium, because it is strongly related to cardiomyocyte contraction; Magnesium, because it is important in the cardiac metabolism; and Iron, because BC treatment induced cardiotoxicity can be associated to the oxidative stress. Changes that occur in unhealthy tissues in case to cardiovascular damages can be better understood when elemental compounds and structures of healthy tissues are known. Low Energy X-ray Fluorescence (LEXRF) technique was used to obtain elemental maps of low Z-elements providing a semi-quantitative analysis of the tissues evaluated under different conditions. Through the technique LEXRF we obtained elemental and absorption maps. The results showed more damages when associating chemotherapy and radiotherapy in comparison to myocardium healthy. Those images taken together with light microscopy, X-ray absorption and phase How to cite this paper: Mantuano, A., Barroso, R.C., Nogueira, L.P., Colaço, M.V., Mota, C.L., Pickler, A., Braz, D., Salata, C., Ferreira-Machado, S., de Almeida, C.E. and 755contrast images, satisfactorily characterize the cardiac tissue for the first time in the literature, from the structural and morphological points of view. LEXRF was carried out at TwinMic beamline in the ELETTRA Synchrotron Facility, at the beamline TwinMic, in Trieste, Italy.

show abstract

“…Iron also accumulates in the atria, but to a lesser extent. When iron content surpasses transferrin‐binding capacity and hemosiderin/ferritin‐storage capability, formation of toxic free unbound iron enters the mitochondria and promotes the formation of hydroxyl radicals . This complex biochemical process culminates in gene alteration, cell apoptosis, and the potential for fibrosis formation.…”

Section: Thalassemia Iron and The Heartmentioning

confidence: 99%

“…Mild to moderate iron overload is ascribed to T2* values ranging from 10 to 20 ms. Severe cardiac siderosis is associated with T2* values <10 ms …”

Section: Assessing the Heart In β‐Thalassemia Major: The Role Of Cmrmentioning

confidence: 99%

“…Although the prevalence of 3T scanners is increasing, there is rather little clinical experience with T2* assessment at 3 T. Early work has demonstrated higher incidence of artifacts at 3 T, impairing T2* measurement quality . There is also a substantial shortening of the T2* time at 3 T, which means that 3T values are not comparable with those found at 1.5 T. Therefore, T2* assessment is currently only recommended at 1.5 T . The first T2* assessment by CMR should be performed as soon as a child with TM can undergo a scan without sedation, typically between the age of 6 and 10 years.…”

Section: Assessing the Heart In β‐Thalassemia Major: The Role Of Cmrmentioning

confidence: 99%

See 1 more Smart Citation

Cardiac complications in thalassemia major

Auger

Pennell

2016

Annals of the New York Academy of Sciences

View full text Add to dashboard Cite

The myocardium is particularly susceptible to complications from iron loading in thalassemia major. In the first years of life, severe anemia leads to high-output cardiac failure and death if not treated. The necessary supportive blood transfusions create loading of iron that cannot be naturally excreted, and this iron accumulates within tissues, including the heart. Free unbound iron catalyzes the formation of toxic hydroxyl radicals, which damage cells and cause cardiac dysfunction. Significant cardiac siderosis may present by the age of 10 and may lead to acute clinical heart failure, which must be treated urgently. Atrial fibrillation is the most frequently encountered iron-related arrhythmia. Iron chelation is effective at removing iron from the myocardium, at the expense of side effects that hamper compliance to therapy. Monitoring of myocardial iron content is mandatory for clinical management of cardiac risk. T2* cardiac magnetic resonance measures myocardial iron and is the strongest biomarker for prediction of heart failure and arrhythmic events. It has been calibrated to human myocardial tissue iron concentration and is highly reproducible across all magnetic resonance scanner vendors. As survival and patient age increases, endothelial dysfunction and diabetes may become new factors in the cardiovascular health of thalassemia patients. Promising new imaging technology and therapies could ameliorate the long-term prognosis.

show abstract

Iron-Induced Damage in Cardiomyopathy: Oxidative-Dependent and Independent Mechanisms

Cited by 131 publications

References 95 publications

Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

Alterations in Low-Z Elements Distribution in Heart Tissue after Treatments to Breast Cancer Using LEXRF Technique

Cardiac complications in thalassemia major

Contact Info

Product

Resources

About