Please confirm you are human (Sign Up for free to never see this)
← Back to Search
Mitochondrial Oxidative Stress, DNA Damage, And Heart Failure.
H. Tsutsui, T. Ide, S. Kinugawa
Published 2006 · Biology, Medicine
Save to my Library
Download PDFAnalyze on Scholarcy
Recent experimental and clinical studies have suggested that oxidative stress is enhanced in heart failure. The production of oxygen radicals is increased in the failing heart, whereas antioxidant enzyme activities are preserved as normal. Mitochondrial electron transport is an enzymatic source of oxygen radical generation and also a target of oxidant-induced damage. Chronic increases in oxygen radical production in the mitochondria can lead to a catastrophic cycle of mitochondrial DNA (mtDNA) damage as well as functional decline, further oxygen radical generation, and cellular injury. Reactive oxygen species induce myocyte hypertrophy, apoptosis, and interstitial fibrosis by activating matrix metalloproteinases. These cellular events play an important role in the development and progression of maladaptive cardiac remodeling and failure. Therefore, mitochondrial oxidative stress and mtDNA damage are good therapeutic targets. Overexpression of mitochondrial transcription factor A (TFAM) could ameliorate the decline in mtDNA copy number and preserve it at a normal level in failing hearts. Consistent with alterations in mtDNA, the decrease in oxidative capacities was also prevented. Therefore, the activation of TFAM expression could ameliorate the pathophysiologic processes seen in myocardial failure. Inhibition of mitochondrial oxidative stress and mtDNA damage could be novel and potentially very effective treatment strategies for heart failure.
This paper references
Mitochondrial DNA mutations and mitochondrial abnormalities in dilated cardiomyopathy.
E. Arbustini (1998)
Matrix metalloproteinase inhibition attenuates early left ventricular enlargement after experimental myocardial infarction in mice.
L. Rohde (1999)
Nuclear receptor signaling and cardiac energetics.
J. Huss (2004)
Inhibition of copper-zinc superoxide dismutase induces cell growth, hypertrophic phenotype, and apoptosis in neonatal rat cardiac myocytes in vitro.
D. Siwik (1999)
Mitochondrial transcription factor A is necessary for mtDNA maintance and embryogenesis in mice
N. Larsson (1998)
Frontotemporal dementia: Neuropil spheroids and presynaptic terminal degeneration
L. Zhou (1998)
The epidemiology of heart failure: the Framingham Study.
K. Ho (1993)
Oxygen free radicals and congestive heart failure.
J. Belch (1991)
Energy metabolism in heart failure
R. Ventura-Clapier (2004)
Buthionine sulfoximine reduces the protective capacity of myocytes to withstand peroxide-derived free radical attack.
C. T. Lê (1993)
Greater susceptibility of failing cardiac myocytes to oxygen free radical-mediated injury.
H. Tsutsui (2001)
Cardiac-Specific Induction of the Transcriptional Coactivator Peroxisome Proliferator-Activated Receptor &ggr; Coactivator-1&agr; Promotes Mitochondrial Biogenesis and Reversible Cardiomyopathy in a Developmental Stage-Dependent Manner
Laurie K. Russell (2004)
Overexpression of Mitochondrial Transcription Factor A Ameliorates Mitochondrial Deficiencies and Cardiac Failure After Myocardial Infarction
M. Ikeuchi (2005)
Mitochondrial DNA maintenance in vertebrates.
G. Shadel (1997)
Oxygen-derived free radicals in postischemic tissue injury.
J. McCord (1985)
Reduced activity of mtTFA decreases the transcription in mitochondria isolated from diabetic rat heart.
A. Kanazawa (2002)
Treatment With Dimethylthiourea Prevents Left Ventricular Remodeling and Failure After Experimental Myocardial Infarction in Mice: Role of Oxidative Stress
S. Kinugawa (2000)
Mitochondrial transcription factor A regulates mtDNA copy number in mammals.
Mats I Ekstrand (2004)
Reduction and Restoration of Mitochondrial DNA Content After Focal Cerebral Ischemia/Reperfusion
H. Chen (2001)
Mitochondrial oxidative stress in heart failure: "oxygen wastage" revisited.
D. Sawyer (2000)
Cardiac involvement in mitochondrial diseases. A study on 17 patients with documented mitochondrial DNA defects.
R. Anan (1995)
Elevated levels of 8-iso-prostaglandin F2alpha in pericardial fluid of patients with heart failure: a potential role for in vivo oxidant stress in ventricular dilatation and progression to heart failure.
Z. Mallat (1998)
Replication and transcription of vertebrate mitochondrial DNA.
D. Clayton (1991)
Right and left myocardial antioxidant responses during heart failure subsequent to myocardial infarction.
M. Hill (1997)
Oxidative stress regulates collagen synthesis and matrix metalloproteinase activity in cardiac fibroblasts.
D. Siwik (2001)
Canaries in the coal mine: mitochondrial DNA and vascular injury from reactive oxygen species.
R. Williams (2000)
Mitochondrial deficiency and cardiac sudden death in mice lacking the MEF2A transcription factor
F. Naya (2002)
Time-dependent changes in matrix metalloproteinase activity and expression during the progression of congestive heart failure: relation to ventricular and myocyte function.
F. Spinale (1998)
Reactive oxygen species produced by macrophage-derived foam cells regulate the activity of vascular matrix metalloproteinases in vitro. Implications for atherosclerotic plaque stability.
S. Rajagopalan (1996)
Increased superoxide in heart failure: a biochemical baroreflex gone awry.
T. Muenzel (1999)
Hydrogen peroxide- and peroxynitrite-induced mitochondrial DNA damage and dysfunction in vascular endothelial and smooth muscle cells.
S. Ballinger (2000)
Antioxidant and oxidative stress changes during heart failure subsequent to myocardial infarction in rats.
M. Hill (1996)
The relationship between somatic mtDNA rearrangements, human heart disease and aging.
O. Kajander (2002)
Mitochondrial gene expression in mammalian striated muscle. Evidence that variation in gene dosage is the major regulatory event.
R. Williams (1986)
Association of mitochondrial DNA damage with aging and coronary atherosclerotic heart disease.
M. Corral-Debrinski (1992)
Mechanisms Controlling Mitochondrial Biogenesis and Respiration through the Thermogenic Coactivator PGC-1
Z. Wu (1999)
Mitochondrial diseases in man and mouse.
D. Wallace (1999)
The biogenesis of mitochondria.
Gottfried Schatz (1970)
Premature ageing in mice expressing defective mitochondrial DNA polymerase
A. Trifunović (2004)
Relationship between the critical level of oxidative stresses and the glutathione peroxidase activity.
O. Toussaint (1993)
Inhibition of mitochondrial gene expression by antisense RNA of mitochondrial transcription factor A (mtTFA)
H. Inagaki (1998)
Mitochondrial electron transport complex I is a potential source of oxygen free radicals in the failing myocardium.
T. Ide (1999)
Depressed mitochondrial transcription factors and oxidative capacity in rat failing cardiac and skeletal muscles
A. Garnier (2003)
Regulation of mitochondrial D‐loops by transcription factor A and single‐stranded DNA‐binding protein
C. Takamatsu (2002)
Nuclear activators and coactivators in mammalian mitochondrial biogenesis.
R. Scarpulla (2002)
Human mitochondrial DNA is packaged with TFAM.
Tanfis Istiaq Alam (2003)
Direct evidence for increased hydroxyl radicals originating from superoxide in the failing myocardium.
T. Ide (2000)
Matrix Metalloproteinase Inhibition After Myocardial Infarction: A New Approach to Prevent Heart Failure?
E. Creemers (2001)
Time-Dependent and Tissue-Specific Accumulation of mtDNA and Respiratory Chain Defects in Chronic Doxorubicin Cardiomyopathy
D. Lebrecht (2003)
Mitochondrial DNA Damage and Dysfunction Associated With Oxidative Stress in Failing Hearts After Myocardial Infarction
T. Ide (2001)
Overexpression of Glutathione Peroxidase Prevents Left Ventricular Remodeling and Failure After Myocardial Infarction in Mice
T. Shiomi (2004)
Transcriptional co-activator PGC-1α drives the formation of slow-twitch muscle fibres
J. Lin (2002)
Dilated cardiomyopathy and atrioventricular conduction blocks induced by heart-specific inactivation of mitochondrial DNA gene expression
J. Wang (1999)
Hydroxyl radical generation during mitochondrial electron transfer and the formation of 8-hydroxydesoxyguanosine in mitochondrial DNA.
C. Giulivi (1995)
Endothelial dysfunction in chronic myocardial infarction despite increased vascular endothelial nitric oxide synthase and soluble guanylate cyclase expression: role of enhanced vascular superoxide production.
J. Bauersachs (1999)
This paper is referenced by
Procédés pour la prévention ou le traitement de l'insuffisance cardiaque
Peter S Rabinovitch (2010)
HIGHLIGHTED TOPIC Perspectives in Innate and Acquired Cardioprotection Aging and cardioprotection
Arshad Jahangir (2007)
Proteome Turnover in Mouse Aging: In Vivo Studies by Stable Isotope Mass Spectrometry
Natan Basisty (2015)
A comprehensive review of the bioenergetics of fatty acid and glucose metabolism in the healthy and failing heart in nondiabetic condition
Ashish Gupta (2017)
Possible molecular mechanisms underlying age-related cardiomyocyte apoptosis in the F344XBN rat heart.
Sunil K. Kakarla (2010)
Cardiac metabolism in hypertrophy and heart failure: implications for therapy
N. Siddiqi (2012)
Cardiovascular Disease, Mitochondria, and Traditional Chinese Medicine
J. Wang (2015)
cardiac cells through mitochondrial dependent and independent pathways
S. Kumar (2012)
Quantification of DNA Damage in Different Tissues in Rats with Heart Failure
G. P. Stefani (2020)
Oxidative stress and autophagy in cardiovascular homeostasis.
C. Morales (2014)
Mitochondrial reactive oxygen species regulate cellular signaling and dictate biological outcomes.
R. Hamanaka (2010)
High glucose-induced Ca2+ overload and oxidative stress contribute to apoptosis of cardiac cells through mitochondrial dependent and independent pathways.
S. Kumar (2012)
Proposed mechanisms for cancer- and treatment-related cognitive changes.
J. Merriman (2013)
Isolevuglandin scavenger attenuates pressure overload-induced cardiac oxidative stress, cardiac hypertrophy, heart failure and lung remodeling.
Linlin Shang (2019)
ROLE OF MITOCHONDRIA DURING BOVINE ADENOVIRUS 3 INFECTION
S. Anand (2011)
CHAPTER 7 HYBRID OPTICAL AND CT IMAGING REVEALS INCREASED MATRIX METALLOPROTEASE ACTIVITY AND APOPTOSIS PRECEDING CARDIAC FAILURE IN PROGEROID ERCC 1 MICE
B. V. Thiel (2018)
Depletion of cellular glutathione modulates LIF-induced JAK1-STAT3 signaling in cardiac myocytes.
M. Kurdi (2012)
The Effects of Olive Leaf Extract on Antioxidant Enzymes Activity and Tumor Growth in Breast Cancer
Sarah Milanizadeh (2014)
Thiol-based mechanisms of the thioredoxin and glutaredoxin systems: implications for diseases in the cardiovascular system.
C. Berndt (2007)
TNF-induced mitochondrial damage: a link between mitochondrial complex I activity and left ventricular dysfunction.
N. Mariappan (2009)
Bioenergetics of the failing heart.
R. Ventura-Clapier (2011)
Glutaredoxin-2 controls cardiac mitochondrial dynamics and energetics in mice, and protects against human cardiac pathologies
Georges N. Kanaan (2018)
Deletion of peroxiredoxin 6 potentiates lipopolysaccharide-induced acute lung injury in mice*
D. Yang (2011)
Iron-rich air pollution nanoparticles: An unrecognised environmental risk factor for myocardial mitochondrial dysfunction and cardiac oxidative stress
B.A. Maher (2020)
Defective DNA Replication Impairs Mitochondrial Biogenesis In Human Failing Hearts
Georgios Karamanlidis (2010)
Taxol, a Microtubule Stabilizer, Improves Cardiac Contractile Function during Ischemia in vitro
Junjie Xiao (2010)
8-Hydroxy-2′-Deoxyguanosine and Cardiovascular Disease: a Systematic Review
L. J. Kroese (2014)
Apolipoprotein-J prevention of fetal cardiac myoblast apoptosis induced by ethanol.
Y. Li (2007)
Protection of peroxiredoxin II on oxidative stress-induced cardiomyocyte death and apoptosis
Wen Zhao (2008)
Relationship between air pollution and hospitalizations for congestive heart failure in elderly people in the city of São Paulo
Ysabely Aguiar Pontes Pamplona (2020)
Effect of dietary selenium on the progression of heart failure in the ageing spontaneously hypertensive rat.
Robyn Lymbury (2010)
Cardiac Mitochondrial Adaptations Induced by Elevated Lipid Exposure
Cynthia Rocha (2015)See more