Heme Oxygenase-1: Clinical Relevance in Ischemic Stroke

Bereczki, Dániel; Balla, József

doi:10.2174/1381612824666180717101104

Cited by 45 publications

(45 citation statements)

References 107 publications

(107 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Another possible target for future therapies is Heme-oxygenase-1 (HO-1); the production of this enzyme is promoted by the transcription agent “nuclear factor erythroid 2-related factor 2” (Nrf2) after an oxidative injury. HO-1 can degrade heme with a consequent release of carbon monoxide (CO), biliverdin-IXa and ferrous iron (Fe 2+ ) [ 183 ]. These molecules seem to play an anti-inflammatory and anti-apoptotic role [ 184 , 185 , 186 , 187 , 188 ].…”

Section: Potential Treatment Strategies In Neuroinflammation Aftementioning

confidence: 99%

Neuroinflammatory Mechanisms in Ischemic Stroke: Focus on Cardioembolic Stroke, Background, and Therapeutic Approaches

Maida

Norrito

Daidone

et al. 2020

IJMS

409

266

View full text Add to dashboard Cite

One of the most important causes of neurological morbidity and mortality in the world is ischemic stroke. It can be a result of multiple events such as embolism with a cardiac origin, occlusion of small vessels in the brain, and atherosclerosis affecting the cerebral circulation. Increasing evidence shows the intricate function played by the immune system in the pathophysiological variations that take place after cerebral ischemic injury. Following the ischemic cerebral harm, we can observe consequent neuroinflammation that causes additional damage provoking the death of the cells; on the other hand, it also plays a beneficial role in stimulating remedial action. Immune mediators are the origin of signals with a proinflammatory position that can boost the cells in the brain and promote the penetration of numerous inflammatory cytotypes (various subtypes of T cells, monocytes/macrophages, neutrophils, and different inflammatory cells) within the area affected by ischemia; this process is responsible for further ischemic damage of the brain. This inflammatory process seems to involve both the cerebral tissue and the whole organism in cardioembolic stroke, the stroke subtype that is associated with more severe brain damage and a consequent worse outcome (more disability, higher mortality). In this review, the authors want to present an overview of the present learning of the mechanisms of inflammation that takes place in the cerebral tissue and the role of the immune system involved in ischemic stroke, focusing on cardioembolic stroke and its potential treatment strategies.

show abstract

Section: Potential Treatment Strategies In Neuroinflammation Aftementioning

confidence: 99%

Neuroinflammatory Mechanisms in Ischemic Stroke: Focus on Cardioembolic Stroke, Background, and Therapeutic Approaches

Maida

Norrito

Daidone

et al. 2020

IJMS

409

266

View full text Add to dashboard Cite

show abstract

“…HO-1 degrades heme through a series of catabolic steps that yield products including biliverdin, carbon monoxide (CO) and free iron ( Gozzelino et al., 2010 ). These effects have sparked interest into multitudes of studies for incorporation into therapeutic regimens for a plausible impediment of disease progression in various inflammatory diseases, CVD and metabolic dysregulation associated with obesity ( Durante, 2003 ; Pae and Chung, 2009 ; Bereczki et al., 2018 ).…”

Section: Antioxidants In Ameliorating Obesity and Associated Comorbidmentioning

confidence: 99%

Therapeutic Efficacy of Antioxidants in Ameliorating Obesity Phenotype and Associated Comorbidities

et al. 2020

View full text Add to dashboard Cite

Obesity has been a worldwide epidemic for decades. Despite the abundant increase in knowledge regarding the etiology and pathogenesis of obesity, the prevalence continues to rise with estimates predicting considerably higher numbers by the year 2030. Obesity is characterized by an abnormal lipid accumulation, however, the physiological consequences of obesity are far more concerning. The development of the obesity phenotype constitutes dramatic alterations in adipocytes, along with several other cellular mechanisms which causes substantial increase in systemic oxidative stress mediated by reactive oxygen species (ROS). These alterations promote a chronic state of inflammation in the body caused by the redox imbalance. Together, the systemic oxidative stress and chronic inflammation plays a vital role in maintaining the obese state and exacerbating onset of cardiovascular complications, Type II diabetes mellitus, dyslipidemia, non-alcoholic steatohepatitis, and other conditions where obesity has been linked as a significant risk factor. Because of the apparent role of oxidative stress in the pathogenesis of obesity, there has been a growing interest in attenuating the pro-oxidant state in obesity. Hence, this review aims to highlight the therapeutic role of antioxidants, agents that negate pro-oxidant state of cells, in ameliorating obesity and associated comorbidities. More specifically, this review will explore how various antioxidants target unique and diverse pathways to exhibit an antioxidant defense mechanism.

show abstract

“…The heme oxygenase-1 family is composed of three iso-enzymes: two constitutive ones form the heme oxygenase-2 and -3 and an inducible one forms heme oxygenase-1. These enzymes catalyze the degradation of heme groups into equimolar amounts of biliverdin, ferrous iron and carbon monoxide [93]. Under diabetic conditions, the heme oxygenase-1 protects retinal endothelial cells exposed to elevated glucose or OS and NSS conditions.…”

Section: Diabetic Retinopathymentioning

confidence: 99%

Nitrosative Stress and Its Association with Cardiometabolic Disorders

et al. 2020

View full text Add to dashboard Cite

Reactive nitrogen species (RNS) are formed when there is an abnormal increase in the level of nitric oxide (NO) produced by the inducible nitric oxide synthase (iNOS) and/or by the uncoupled endothelial nitric oxide synthase (eNOS). The presence of high concentrations of superoxide anions (O2−) is also necessary for their formation. RNS react three times faster than O2− with other molecules and have a longer mean half life. They cause irreversible damage to cell membranes, proteins, mitochondria, the endoplasmic reticulum, nucleic acids and enzymes, altering their activity and leading to necrosis and to cell death. Although nitrogen species are important in the redox imbalance, this review focuses on the alterations caused by the RNS in the cellular redox system that are associated with cardiometabolic diseases. Currently, nitrosative stress (NSS) is implied in the pathogenesis of many diseases. The mechanisms that produce damage remain poorly understood. In this paper, we summarize the current knowledge on the participation of NSS in the pathology of cardiometabolic diseases and their possible mechanisms of action. This information might be useful for the future proposal of anti-NSS therapies for cardiometabolic diseases.

show abstract

Heme Oxygenase-1: Clinical Relevance in Ischemic Stroke

Cited by 45 publications

References 107 publications

Neuroinflammatory Mechanisms in Ischemic Stroke: Focus on Cardioembolic Stroke, Background, and Therapeutic Approaches

Neuroinflammatory Mechanisms in Ischemic Stroke: Focus on Cardioembolic Stroke, Background, and Therapeutic Approaches

Therapeutic Efficacy of Antioxidants in Ameliorating Obesity Phenotype and Associated Comorbidities

Nitrosative Stress and Its Association with Cardiometabolic Disorders

Contact Info

Product

Resources

About