Mitochondrial pathology in cardiac failure

Marı́n-Garcı́a, José

doi:10.1016/s0008-6363(00)00241-8

Cited by 122 publications

(79 citation statements)

References 104 publications

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“…From the results presented here, we speculate that mitochondrial dysfunction in heart failure (Marin-Garcia et al, 2001) produces an inward-rectifier K ϩ -channel inhibitor that is responsible for reducing the cardiac inward-rectifier current (Beuckelmann et al, 1993;Kaab et al, 1996;Lodge and Normandin, 1997;Han et al, 2001), thereby contributing to an increased risk of arrhythmia (Pogwizd et al, 2001). Furthermore, we speculate that the inhibitor bears a positive charge, because the presence of a positive charge in or near the binding site would be expected to decrease the affinity of the channel for the positively charged moiety of the inhibitory ligand.…”

Section: Discussionmentioning

confidence: 93%

“…Mitochondrial dysfunction is increasingly recognized as an important aspect of the pathophysiology of several neurological and cardiovascular disorders, including Alzheimer's disease (Baloyannis et al, 2004), Parkinson's disease (Fiskum et al, 2003), heart failure (Marin-Garcia et al, 2001), myocardial and cerebral ischemia (Sims and Anderson, 2002;Sadek et al, 2003), and, potentially, epilepsy (Patel, 2002). Alteration of electrical excitability is central to many of these diseases, leading to either neuronal excitotoxicity or cardiac arrhythmia (Doble, 1999;Janse, 2004).…”

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confidence: 99%

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Differential Sensitivity of K_ir2 Inward-Rectifier Potassium Channels to a Mitochondrial Uncoupler: Identification of a Regulatory Site

Collins

Wang²,

Larson³

2005

Mol Pharmacol

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The aim of this study was to gain insight into the mechanism by which members of the K ir 2 subfamily are differentially sensitive to agents that inhibit mitochondrial function by identifying responsible site(s) in K ir 2 proteins. K ir 2 channels were expressed in Xenopus laevis oocytes and assayed by two-electrode voltage clamp and patch clamp. Incubation of oocytes in carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP), a mitochondrial uncoupler,

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Section: Discussionmentioning

confidence: 93%

mentioning

confidence: 99%

Differential Sensitivity of K_ir2 Inward-Rectifier Potassium Channels to a Mitochondrial Uncoupler: Identification of a Regulatory Site

Collins

Wang²,

Larson³

2005

Mol Pharmacol

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“…In two studies with humans and one study with mice, we found this mutation to predominate, representing from 55 to 62 percent of total mutations seen in the three studies (11,12,13). Thus, it appears likely that natural mitochondrial dNTP asymmetry, at least in heart and skeletal muscle, influences the spontaneous mutation rate and spectrum.…”

Section: Stimulation Of Mitochondrial Mutagenesis By Dntp Pool Imbalancementioning

confidence: 77%

DNA Precursor Metabolism and Mitochondrial Genome Stability

Mathews¹

2003

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Public Reporting Burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing the collection of information. ABSTRACTThis project investigated DNA precursor metabolism in mammalian mitochondria, attempting to define relationships between deoxyribonucleoside triphosphate (dNTP) metabolism and mutagenesis in the mitochondrial genome. Specific contributions include: (1) We found that conditions altering the normal balance among the four dNTP pools within the mitochondrion stimulate both point and deletion mutagenesis; (2) dNTP pools in mitochondria from some tissues are highly asymmetric, and this asymmetry contributes toward the elevation of mitochondrial mutation rates compared to nuclear mutation rates; (3) Mitochondrial dNTP pools do not show significant age-related changes in the rat, ruling out such changes as causative agents in aging-related accumulation of mitochondrial mutations; (4) A protein previously identified as a mitochondrial deoxyribonucleotide carrier, responsible for dNTP uptake into mitochondria, plays a quite different metabolic role; (5) Mammalian mitochondria contain a novel ribonucleotide reductase, which may play a significant role in mitochondrial dNTP synthesis.(a) Papers published in peer-reviewed journals (N/A for none)

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“…Independent of the heart failure stage, changes in mitochondrial electron transport chain components were described [134][135][136][137]. Indeed, the progressive decrease of ATP production is linked to both a decrease of fatty acid oxidation and a reduction of mitochondrial respiration due to electron transport chain defects [138].…”

Section: Heart and Oxidative Stressmentioning

confidence: 99%

Free Radicals and Biomarkers Related to the Diagnosis of Cardiorenal Syndrome

Restini¹,

Pereira²,

Geleilete³

2016

Free Radicals and Diseases

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The National Heart, Lung, and Blood Institute Working Group has postulated the cardiorenal syndrome (CRS) as an interaction between the kidneys and the cardiovascular system in which therapy to relieve congestive heart failure (HF) symptoms is limited by the further worsening renal function. CRS is classified from type I to V, taking into account the progression of the symptoms in terms of mechanisms, clinical conditions, and biomarkers. Experimental and clinical studies have shown the kidney as both a trigger and a target to sympathetic nervous system (SNS) overactivity. Renal damage and ischemia, activation of the renin angiotensin aldosterone system (RAAS), and dysfunction of nitric oxide (NO) system are associated with kidney adrenergic activation. Indeed, the imbalances of RAAS and/or SNS share an important common process in CRS: the activation and production of free radicals, especially reactive oxygen species (ROS). The present chapter addresses connections of the free radicals as potential biomarkers as the imbalances in the RAAS and the SNS are developed. Understanding the involvement of free radicals in CRS may bring knowledge to design studies in order to develop accurate pharmacological interventions.

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Mitochondrial pathology in cardiac failure

Cited by 122 publications

References 104 publications

Differential Sensitivity of K_ir2 Inward-Rectifier Potassium Channels to a Mitochondrial Uncoupler: Identification of a Regulatory Site

Differential Sensitivity of K_ir2 Inward-Rectifier Potassium Channels to a Mitochondrial Uncoupler: Identification of a Regulatory Site

DNA Precursor Metabolism and Mitochondrial Genome Stability

Free Radicals and Biomarkers Related to the Diagnosis of Cardiorenal Syndrome

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Mitochondrial pathology in cardiac failure

Cited by 122 publications

References 104 publications

Differential Sensitivity of Kir2 Inward-Rectifier Potassium Channels to a Mitochondrial Uncoupler: Identification of a Regulatory Site

Differential Sensitivity of Kir2 Inward-Rectifier Potassium Channels to a Mitochondrial Uncoupler: Identification of a Regulatory Site

DNA Precursor Metabolism and Mitochondrial Genome Stability

Free Radicals and Biomarkers Related to the Diagnosis of Cardiorenal Syndrome

Contact Info

Product

Resources

About

Differential Sensitivity of K_ir2 Inward-Rectifier Potassium Channels to a Mitochondrial Uncoupler: Identification of a Regulatory Site

Differential Sensitivity of K_ir2 Inward-Rectifier Potassium Channels to a Mitochondrial Uncoupler: Identification of a Regulatory Site