Mitochondria and aging: innocent bystanders or guilty parties?

Tońska, Katarzyna; Sołyga, A.; Bartnik, Ewa

doi:10.1007/bf03195653

Cited by 10 publications

(8 citation statements)

References 54 publications

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“…Indeed, a mammalian cell harbors hundreds to thousands of mitochondria, each containing 2-10 copies of mtDNA encoding components of the electron transport chain. Moreover, mutations in mtDNA have been linked to aging, [239][240][241] hereditary diseases 242,243 and carcinogenesis. 244,245 Mitochondrial DNA is known to be associated with the inner membrane of the organelle and is therefore located in the vicinity of endogenous mitochondrial ROS generated by the nearby respiratory machinery.…”

Section: Dna Glycosylase Biologymentioning

confidence: 99%

Consequences and Repair of Oxidative DNA Damage

Duclos¹,

Doublié²,

Wallace³

2012

The Cellular Response to the Genotoxic Insult

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Section: Dna Glycosylase Biologymentioning

confidence: 99%

Consequences and Repair of Oxidative DNA Damage

Duclos¹,

Doublié²,

Wallace³

2012

The Cellular Response to the Genotoxic Insult

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“…Unexpectedly, mitochondrial ROS generation and mtDNA oxidative damage are not increased in muscles from mtDNA-mutator mice, casting doubts on the validity of the MFRTA, at least in this model of sarcopenia (Kujoth et al, 2005; Hiona and Leeuwenburgh, 2008). Indeed, the possibility exists that in PolG mice the excessive load of mtDNA mutations might lead to the apoptotic elimination of myocytes before oxidative damage to mtDNA becomes detectable (Tonska et al, 2009). It should also be considered that, besides oxidized bases, other forms of nucleic acid damage can be inflicted by ROS, including DNA breaks that can result in deletion mutations.…”

Section: Mitochondria As a Source Of Oxidantsmentioning

confidence: 99%

Mitochondrial pathways in sarcopenia of aging and disuse muscle atrophy

Calvani

Joseph

Adhihetty

et al. 2013

Biological Chemistry

262

203

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Muscle loss during aging and disuse is a highly prevalent and disabling condition, but knowledge about cellular pathways mediating muscle atrophy is still limited. Given the postmitotic nature of skeletal myocytes, the maintenance of cellular homeostasis relies on the efficiency of cellular quality control mechanisms. In this scenario, alterations in mitochondrial function are considered a major factor underlying sarcopenia and muscle atrophy. Damaged mitochondria are not only less bioenergetically efficient, but also generate increased amounts of reactive oxygen species, interfere with cellular quality control mechanisms, and display a greater propensity to trigger apoptosis. Thus, mitochondria stand at the crossroad of signaling pathways that regulate skeletal myocyte function and viability. Studies on these pathways have sometimes provided unexpected and counterintuitive results, which suggests that they are organized into a complex, heterarchical network that is currently insufficiently understood. Untangling the complexity of such a network will likely provide clinicians with novel and highly effective therapeutics to counter the muscle loss associated with aging and disuse. In this review, we summarize the current knowledge on the mechanisms whereby mitochondrial dysfunction intervenes in the pathogenesis of sarcopenia and disuse atrophy, and highlight the prospect of targeting specific processes to treat these conditions.

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“…Human mtDNA defects have been found to accumulate with age and in age-related neurodegenerative diseases, such as Alzheimer's and Parkinson's [42-46] (Figure 1). These defects are known to induce free-radical production and to damage mitochondrial function [47-48].…”

Section: Genetics and Asthmamentioning

confidence: 99%

Mitochondrial Dysfunction and Oxidative Stress in Asthma: Implications for Mitochondria-Targeted Antioxidant Therapeutics

Reddy

2011

Pharmaceuticals

117

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Asthma is a complex, inflammatory disorder characterized by airflow obstruction of variable degrees, bronchial hyper-responsiveness, and airway inflammation. Asthma is caused by environmental factors and a combination of genetic and environmental stimuli. Genetic studies have revealed that multiple loci are involved in the etiology of asthma. Recent cellular, molecular, and animal-model studies have revealed several cellular events that are involved in the progression of asthma, including: increased Th2 cytokines leading to the recruitment of inflammatory cells to the airway, and an increase in the production of reactive oxygen species and mitochondrial dysfunction in the activated inflammatory cells, leading to tissue injury in the bronchial epithelium. Further, aging and animal model studies have revealed that mitochondrial dysfunction and oxidative stress are involved and play a large role in asthma. Recent studies using experimental allergic asthmatic mouse models and peripheral cells and tissues from asthmatic humans have revealed antioxidants as promising treatments for people with asthma. This article summarizes the latest research findings on the involvement of inflammatory changes, and mitochondrial dysfunction/oxidative stress in the development and progression of asthma. This article also addresses the relationship between aging and age-related immunity in triggering asthma, the antioxidant therapeutic strategies in treating people with asthma.

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Mitochondria and aging: innocent bystanders or guilty parties?

Cited by 10 publications

References 54 publications

Consequences and Repair of Oxidative DNA Damage

Consequences and Repair of Oxidative DNA Damage

Mitochondrial pathways in sarcopenia of aging and disuse muscle atrophy

Mitochondrial Dysfunction and Oxidative Stress in Asthma: Implications for Mitochondria-Targeted Antioxidant Therapeutics

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