Role of NO in Myocardial Injury Induced by Oxidative Stress: Ischemia, Myocarditis, Cardiomyopathy, and Heart Failure

Heart Failure ◽  
2000 ◽  
pp. 81-87
Author(s):  
Tsunehiko Kuzuya ◽  
Masashi Nishida
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Myocardial Injury

Role of oxidative stress in left ventricular remodeling and heart failure after myocardial infarction

1999 ◽  
Vol 5 (3) ◽  
pp. 79
Author(s):  
Shintaro Kinugawa ◽  
Hiroyuki Tsutsui ◽  
Tomomi Ide ◽  
Hideo Ustumi ◽  
Nobuhiro Suematsu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Heart Failure ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Left Ventricular

Abstract 125: Perturbation of Mitochondrial Calcium Uniporter Promotes Cardiac Oxidative Stress and Autophagy During Heart Failure

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Sudarsan Rajan ◽  
Santhanam Shanmughapriya ◽  
Dhanendra Tomar ◽  
Zhiwei Dong ◽  
Joseph Y Cheung ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Mouse Model ◽  
Atp Depletion ◽  
Regulatory Role ◽  
Mitochondrial Calcium ◽  
Mitochondrial Bioenergetics ◽  
Complex Assembly ◽  
New Findings

Mitochondrial calcium ([Ca 2+ ] m ) is essential for cardiomyocyte viability, and aberration of [Ca 2+ ] m is known to elicit multiple cardiac stress conditions associated with ATP depletion, reactive oxygen species, and mitochondrial permeability transition pore opening, all of which can lead to metabolic stress and the loss of dysfunctional mitochondria by aberrant autophagy. Elucidating the regulatory role of m itochondrial c alcium u niporter (MCU)-mediated [Ca 2+ ] m in modulating cardiac mitochondrial bioenergetics and autophagy has high significance and clinical impact for many pathophysiological processes. [Ca 2+ ] m is exquisitely controlled by the inner mitochondrial membrane uniporter, transporters, regulators and exchangers including MCU, MCUR1, EMRE, MICU1, MICU2 and LETM1. Our recently published findings revealed that Mitochondrial Ca 2+ Uniporter Regulator 1 (MCUR1) serves as a scaffold factor for uniporter complex assembly. We found that deletion of MCUR1 impaired [Ca 2+ ] m uptake, mitochondrial Ca 2+ current ( I MCU ) and mitochondrial bioenergetics and is associated with increased autophagy. Our new findings indicate that the impairment of [Ca 2+ ] m uptake exacerbated autophagy following ischemia-reperfusion (I/R) injury. In support of our mouse model, human failing hearts show that MCUR1 protein levels are markedly decreased and autophagy markers are increased, demonstrating a crucial link between [Ca 2+ ] m uptake and autophagy during heart failure. Additionally, our results reveal that either oxidation or disruption of human MCU Cys-97 (in mouse Cys-96; gain-of-function MCU C96A mutant) produces a conformational change within the N terminal β-grasp fold of MCU which promotes higher-order MCU complex assembly and increased I MCU activity and mitochondrial ROS levels. The results of our studies using a novel cardiac-specific MCUR1-KO model and a constitutively active global MCU C96A KI mouse model (CRISPR-Cas9 genome edited) elucidate the regulatory role of [Ca 2+ ] m in cardiac bioenergetics and autophagy during oxidative stress and myocardial infarction. Thus, targeting assembly and the activity of MCU complex will offer a new potential therapeutic target in the treatment of cardiomyopathy and heart failure.

scholarly journals Role of Oxidative Stress in Heart Failure: Insights from Gene Transfer Studies

Biomedicines ◽  
2021 ◽  
Vol 9 (11) ◽  
pp. 1645
Author(s):  
Bart De Geest ◽  
Mudit Mishra
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Gene Therapy ◽  
Steady State ◽  
Gene Transfer ◽  
Oxidative Modification ◽  
Heme Oxygenase 1 ◽  
Therapy Studies ◽  
Pathological Remodeling

Under physiological circumstances, there is an exquisite balance between reactive oxygen species (ROS) production and ROS degradation, resulting in low steady-state ROS levels. ROS participate in normal cellular function and in cellular homeostasis. Oxidative stress is the state of a transient or a persistent increase of steady-state ROS levels leading to disturbed signaling pathways and oxidative modification of cellular constituents. It is a key pathophysiological player in pathological hypertrophy, pathological remodeling, and the development and progression of heart failure. The heart is the metabolically most active organ and is characterized by the highest content of mitochondria of any tissue. Mitochondria are the main source of ROS in the myocardium. The causal role of oxidative stress in heart failure is highlighted by gene transfer studies of three primary antioxidant enzymes, thioredoxin, and heme oxygenase-1, and is further supported by gene therapy studies directed at correcting oxidative stress linked to metabolic risk factors. Moreover, gene transfer studies have demonstrated that redox-sensitive microRNAs constitute potential therapeutic targets for the treatment of heart failure. In conclusion, gene therapy studies have provided strong corroborative evidence for a key role of oxidative stress in pathological remodeling and in the development of heart failure.

scholarly journals The Role of Oxidative Stress in Cardiac Disease: From Physiological Response to Injury Factor

2020 ◽  
Vol 2020 ◽  
pp. 1-29 ◽  
Author(s):  
Rossella D’Oria ◽  
Rossella Schipani ◽  
Anna Leonardini ◽  
Annalisa Natalicchio ◽  
Sebastio Perrini ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Injury ◽  
Antioxidant Defense ◽  
Experimental Studies ◽  
Chemical Species ◽  
Oxygen Species ◽  
Molecular Abnormalities ◽  
Defense Systems ◽  
Antioxidant Defense Systems

Reactive oxygen species (ROS) are highly reactive chemical species containing oxygen, controlled by both enzymatic and nonenzymatic antioxidant defense systems. In the heart, ROS play an important role in cell homeostasis, by modulating cell proliferation, differentiation, and excitation-contraction coupling. Oxidative stress occurs when ROS production exceeds the buffering capacity of the antioxidant defense systems, leading to cellular and molecular abnormalities, ultimately resulting in cardiac dysfunction. In this review, we will discuss the physiological sources of ROS in the heart, the mechanisms of oxidative stress-related myocardial injury, and the implications of experimental studies and clinical trials with antioxidant therapies in cardiovascular diseases.

The role of metabolism disorders, inflammation, myocardial injury in development chronic heart failure in metabolic syndrome patients

2018 ◽  
Vol 7 (4) ◽  
pp. 5
Author(s):  
A. P. Roytman ◽  
T. A. Fedorova ◽  
E. A. Ivanova ◽  
A. V. Bugrov ◽  
V. V. Dolgov
Keyword(s):  
Heart Failure ◽  
Metabolic Syndrome ◽  
Chronic Heart Failure ◽  
Myocardial Injury

Novel Role of AT1 Receptor in Heart Failure and the Significance of Oxidative Stress

2006 ◽  
Vol 12 (8) ◽  
pp. S152
Author(s):  
Shokei Kim-Mitsuyama ◽  
Eiichiro Yamamoto
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
At1 Receptor

scholarly journals Pathophysiological role of oxidative stress in systolic and diastolic heart failure and its therapeutic implications

2015 ◽  
Vol 36 (38) ◽  
pp. 2555-2564 ◽  
Author(s):  
Thomas Münzel ◽  
Tommaso Gori ◽  
John F. Keaney ◽  
Christoph Maack ◽  
Andreas Daiber
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Diastolic Heart Failure ◽  
Therapeutic Implications ◽  
Pathophysiological Role

scholarly journals Oxidative Stress in Heart Failure: The Role of Mitochondria.

2001 ◽  
Vol 40 (12) ◽  
pp. 1177-1182 ◽  
Author(s):  
Hiroyuki TSUTSUI
Keyword(s):  
Oxidative Stress ◽  
Heart Failure
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