Bioenergetic Origins of Complexity and Disease

Wallace, D C

doi:10.1101/sqb.2011.76.010462

Cited by 111 publications

(88 citation statements)

References 133 publications

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“…Mitochondria is likely to be a major focal point for the generation of reactive oxygen species (16)(17)(18)(19). In addition, oxygen insufficiency results in decreased mitochondrial function resulting in altered cellular energetics.…”

Section: Introductionmentioning

confidence: 99%

Resveratrol Improves Survival and Prolongs Life Following Hemorrhagic Shock

Ayub

Poulose

Raju

2015

Mol Med

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Resveratrol has been shown to potentiate mitochondrial function and extend longevity; however, there is no evidence to support whether resveratrol can improve survival or prolong life following hemorrhagic shock. We sought to determine whether (a) resveratrol can improve survival following hemorrhage and resuscitation and (b) prolong life in the absence of resuscitation. Using a hemorrhagic injury (HI) model in the rat, we describe for the first time that the naturally occurring small molecule, resveratrol, may be an effective adjunct to resuscitation fluid. In a series of three sets of experiments we show that resveratrol administration during resuscitation improves survival following HI (p < 0.05), resveratrol and its synthetic mimic SRT1720 can significantly prolong life in the absence of resuscitation fluid (<30 min versus up to 4 h; p < 0.05), and resveratrol as well as SRT1720 restores left ventricular function following HI. We also found significant changes in the expression level of mitochondria-related transcription factors Ppar-α and Tfam, as well as Pgc-1α in the left ventricular tissues of rats subjected to HI and treated with resveratrol. The results indicate that resveratrol is a strong candidate adjunct to resuscitation following severe hemorrhage.

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Section: Introductionmentioning

confidence: 99%

Resveratrol Improves Survival and Prolongs Life Following Hemorrhagic Shock

Ayub

Poulose

Raju

2015

Mol Med

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“…It can cause neurodegeneration (13), and ultimately results in programmed cell death (14,15). Programmed cell death is triggered by the release of apoptogens, such as cytochrome c (cyt-c), through pores that open in the outer mitochondrial membrane (16).…”

mentioning

confidence: 99%

Age-dependent dissociation of ATP synthase dimers and loss of inner-membrane cristae in mitochondria

Daum

Walter

Horst

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

213

195

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Aging is one of the most fundamental, yet least understood biological processes that affect all forms of eukaryotic life. Mitochondria are intimately involved in aging, but the underlying molecular mechanisms are largely unknown. Electron cryotomography of whole mitochondria from the aging model organism Podospora anserina revealed profound age-dependent changes in membrane architecture. With increasing age, the typical cristae disappear and the inner membrane vesiculates. The ATP synthase dimers that form rows at the cristae tips dissociate into monomers in inner-membrane vesicles, and the membrane curvature at the ATP synthase inverts. Dissociation of the ATP synthase dimer may involve the peptidyl prolyl isomerase cyclophilin D. Finally, the outer membrane ruptures near large contact-site complexes, releasing apoptogens into the cytoplasm. Inner-membrane vesiculation and dissociation of ATP synthase dimers would impair the ability of mitochondria to supply the cell with sufficient ATP to maintain essential cellular functions.subtomogram averaging | cell death

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“…PD, for instance, is a neurodegenerative disorder characterized, in part, by the progressive and selective loss of DA-ergic neuron cell bodies within the SNc and the associated deficiency of DA in the striatum, which gives rise to the typical motor symptoms. Data from epidemiological studies in humans and molecular studies in genetic, as well as in toxin-induced animal models of PD, indicate that mitochondrial dysfunction and oxidative stress occurs early in the pathogenesis of this neurodegenerative disorder [64].…”

Section: Redox-mediated Modulation Of Th Activitymentioning

confidence: 99%

Redox Sensitivity of Tyrosine Hydroxylase Activity and Expression in Dopaminergic Dysfunction

Giovanni

Pessia²,

Maio³

2012

CNSNDDT

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Oxidant molecules generated during neuronal metabolism appear to play a significant role in the processes of aging and neurodegeneration. Increasing experimental evidence suggests the noteworthy relevance of the intracellular reduction-oxidation (redox) balance for the dopaminergic (DA-ergic) neurons of the substantia nigra pars compacta. These cells possess a distinct physiology intrinsically associated with elevated reactive oxygen species production, conferring on them a high vulnerability to free radical damage, one of the major causes of selective DA-ergic neuron dysfunction and degeneration related to neurological disorders such as Parkinson's disease. Tyrosine hydroxylase (tyrosine 3-monooxygenase; E.C. 1.14.16.2; TH) activity represents the rate-limiting biochemical event in DA synthesis. TH activity, metabolism and expression are finely tuned by several regulatory systems in order to maintain a crucial physiological condition in which DA synthesis is closely coupled to its secretion. Alterations of these regulatory systems of TH functions have indeed been thought to be key events in the DA-ergic degeneration. TH has seven cysteine residues presenting thiols. Depending on the oxido-reductive (redox) status of the cellular environment, thiols exist either in the reduced form of free thiols or oxidized to disulfides. The formation of disulfides in proteins exerts critical regulatory functions both in physiological and in pathological conditions when oxidative stress is sustained. Several reports have recently shown that redox state changes of thiol residues, as consequence of an oxidative injury, can directly or indirectly affect the TH activity, metabolism and expression.The major focus of this review, therefore, is to report recent evidence on the redox modulation of TH activity and expression, and to provide an overview of a cellular phenomenon that might represent a target for new therapeutic strategies against the DA-ergic neurodegenerative disorders.

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Bioenergetic Origins of Complexity and Disease

Cited by 111 publications

References 133 publications

Resveratrol Improves Survival and Prolongs Life Following Hemorrhagic Shock

Resveratrol Improves Survival and Prolongs Life Following Hemorrhagic Shock

Age-dependent dissociation of ATP synthase dimers and loss of inner-membrane cristae in mitochondria

Redox Sensitivity of Tyrosine Hydroxylase Activity and Expression in Dopaminergic Dysfunction

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