Mitochondrial impairment contributes to cocaine-induced cardiac dysfunction: Prevention by the targeted antioxidant MitoQ

Vergeade, Aurélia; Mulder, Paul; Vendeville-Dehaudt, Cathy; Estour, François; Fortin, D.; Ventura‐Clapier, Renée; Thuillez, Christian; Monteil, Christelle

doi:10.1016/j.freeradbiomed.2010.05.024

Cited by 61 publications

(51 citation statements)

References 43 publications

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“…These authors conclude that the reduced synthesis rate of mitochondrial proteins in response to ethanol exposure may be partly connected to depression in myocardial contractility and associated with functional damage of mitochondrial metabolism (120). In contrast, cocaine-induced cardiac dysfunction in rats revealed increased ROS production and decreased ATP synthesis in the IFM (137), which may occur through a xanthine oxidase-mediated mechanism (138). Hence, the majority of studies investigating the effects of drugs on mitochondrial subpopulations implicate SSM as being primarily affected.…”

Section: Pathological Influencementioning

confidence: 95%

Physiological and structural differences in spatially distinct subpopulations of cardiac mitochondria: influence of cardiac pathologies

Hollander

Thapa

Shepherd

2014

American Journal of Physiology-Heart and Circulatory Physiology

130

118

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Section: Pathological Influencementioning

confidence: 95%

Physiological and structural differences in spatially distinct subpopulations of cardiac mitochondria: influence of cardiac pathologies

Hollander

Thapa

Shepherd

2014

American Journal of Physiology-Heart and Circulatory Physiology

130

118

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“…Complex I seems to be a direct target of cocaine in rat brain mitochondria (Cunha-Oliveira et al, 2013d;Dietrich et al, 2004), and also in heart (Vergeade et al, 2010;Yuan & Acosta, 1996, 2000 and liver mitochondria (Cunha-Oliveira et al, 2013c;Devi & Chan, 1997). In vitro exposure to cocaine was shown to affect the respiratory chain in different manners in liver and brain FIGURE 21.2 Interactions of cocaine with mitochondrial functions.…”

Section: Part | III Cellular Effectsmentioning

confidence: 99%

“…Oxidative stress may be a consequence of cocaineinduced mitochondrial dysfunction, but it may also be a factor involved in cocaine's mitochondrial effects (Vergeade et al, 2010).…”

Section: Part | III Cellular Effectsmentioning

confidence: 99%

Role of Mitochondria on the Neurological Effects of Cocaine

Pereira

Cunha‐Oliveira

2017

The Neuroscience of Cocaine

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“…Indeed, the development of antioxidant molecules that achieve concentrations in mitochondria 100-to 1,000-fold higher than in the cytosol, such as Szeto-Schiller (SS) synthetic antioxidant peptides (26,178,179,230), MitoQ (176,205), and Euk-8 (a SOD/catalase mimetic and antioxidant) (94,202), have demonstrated some efficacy in models of cardiovascular stress. A recent study in spontaneous hypertensive rats showed that MitoQ treatment for 8 weeks significantly reduced systolic blood pressure, improved endothelial function, and attenuated cardiac hypertrophy (64).…”

Section: Mitochondrial Dysfunction As a Pharmacological Target Againsmentioning

confidence: 99%

Role of mitochondrial dysfunction and altered autophagy in cardiovascular aging and disease: from mechanisms to therapeutics

Marzetti

Csiszár

Dutta

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

170

131

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Advanced age is associated with a disproportionate prevalence of cardiovascular disease (CVD). Intrinsic alterations in the heart and the vasculature occurring over the life course render the cardiovascular system more vulnerable to various stressors in late life, ultimately favoring the development of CVD. Several lines of evidence indicate mitochondrial dysfunction as a major contributor to cardiovascular senescence. Besides being less bioenergetically efficient, damaged mitochondria also produce increased amounts of reactive oxygen species, with detrimental structural and functional consequences for the cardiovascular system. The agerelated accumulation of dysfunctional mitochondrial likely results from the combination of impaired clearance of damaged organelles by autophagy and inadequate replenishment of the cellular mitochondrial pool by mitochondriogenesis. In this review, we summarize the current knowledge about relevant mechanisms and consequences of age-related mitochondrial decay and alterations in mitochondrial quality control in the cardiovascular system. The involvement of mitochondrial dysfunction in the pathogenesis of cardiovascular conditions especially prevalent in late life and the emerging connections with neurodegeneration are also illustrated. Special emphasis is placed on recent discoveries on the role played by alterations in mitochondrial dynamics (fusion and fission), mitophagy, and their interconnections in the context of age-related CVD and endothelial dysfunction. Finally, we discuss pharmacological interventions targeting mitochondrial dysfunction to delay cardiovascular aging and manage CVD. oxidative stress; mitophagy; fusion and fission; neurodegeneration; resveratrol THIS ARTICLE is part of a collection on Mitochondria in Cardiovascular Physiology and Disease. Other articles appearing in this collection, as well as a full archive of all collections, can be found online at http://ajpheart.physiology.org/.Advanced age is associated with excessive incidence and prevalence of cardiovascular disease (CVD). Over 80% of cases of coronary artery disease (CAD) and more than 75% of those of congestive heart failure (CHF) are observed in elderly patients (113). The incidence of CVD, including CAD, CHF, and stroke, increases from 4 -10/1,000 person-years in adults aged 45-54 years to 65-75/1,000 person-years in those older than 85 (112). CVD is also a major cause of chronic disability in advanced age (140). Indeed, subclinical CVD is associated with a decline in physical and cognitive function equivalent to over 5 years of aging (136). Similarly, neurodegenerative disorders, such as vascular dementia and Alzheimer's disease (AD), pose a major problem to global public health (45,90).Although the long-term exposure to cardiovascular risk factors plays a major role in the etiopathogenesis of CVD and neurodegeneration, intrinsic aging of the heart and the vasculature greatly enhances the susceptibility to developing CVD and neurodegenerative conditions in late life (100). The cardiovascular sy...

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Mitochondrial impairment contributes to cocaine-induced cardiac dysfunction: Prevention by the targeted antioxidant MitoQ

Cited by 61 publications

References 43 publications

Physiological and structural differences in spatially distinct subpopulations of cardiac mitochondria: influence of cardiac pathologies

Physiological and structural differences in spatially distinct subpopulations of cardiac mitochondria: influence of cardiac pathologies

Role of Mitochondria on the Neurological Effects of Cocaine

Role of mitochondrial dysfunction and altered autophagy in cardiovascular aging and disease: from mechanisms to therapeutics

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