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Open AccessJournal ArticleDOI

Hypermetabolism and hypercatabolism of skeletal muscle accompany mitochondrial stress following severe burn trauma

TLDR
It is found that burn patients were profoundly hypermetabolic at both the skeletal muscle and systemic levels, indicating increased oxygen consumption by mitochondria and a novel role for the mitochondria in burn-induced cachexia.
Abstract
Burn trauma results in prolonged hypermetabolism and skeletal muscle wasting. How hypermetabolism contributes to muscle wasting in burn patients remains unknown. We hypothesized that oxidative stre...

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Nutraceuticals and Exercise against Muscle Wasting during Cancer Cachexia

TL;DR: This review focuses on the current state of the field on the role of inflammation and OS in the pathogenesis of muscle atrophy during CC, and how nutraceuticals and physical activity may act synergistically to limit muscle wasting and dysfunction.
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Metabolismo y terapia nutricional en el paciente quemado crítico: una revisión actualizada

TL;DR: En las ultimas 4 decadas se han estudiado diferentes intervenciones nutricionales y farmacologicas moduladoras de la respuesta inmune y metabolica, y dichas estrategias han demostrado ser capaces de minimizar the malnutricion aguda, modular the respUesta inmunoinflamatoria y mejorar los resultados clinicos.
References
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Journal ArticleDOI

How mitochondria produce reactive oxygen species.

TL;DR: The description outlined here facilitates the understanding of factors that favour mitochondrial ROS production and develops better methods to measure mitochondrial O2•− and H2O2 formation in vivo, as uncertainty about these values hampers studies on the role of mitochondrial ROS in pathological oxidative damage and redox signalling.
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New methods for calculating metabolic rate with special reference to protein metabolism.

TL;DR: Several ways in which the calculation of metabolic rate by indirect calorimetry can be simplified are described and how the effect of protein metabolism can be included with a minimum of trouble are shown.
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Mitochondrial formation of reactive oxygen species.

TL;DR: This review describes the main mitochondrial sources of reactive species and the antioxidant defences that evolved to prevent oxidative damage in all the mitochondrial compartments and discusses various physiological and pathological scenarios resulting from an increased steady state concentration of mitochondrial oxidants.
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Nitric oxide, oxidants, and protein tyrosine nitration

TL;DR: Although protein tyrosine nitration is a low-yield process in vivo, 3-nitrotyrosine has been revealed as a relevant biomarker of •NO-dependent oxidative stress; additionally, site-specific nitration focused on particularprotein tyrosines may result in modification of function and promote a biological effect.
Journal ArticleDOI

Protein Degradation by the Ubiquitin–Proteasome Pathway in Normal and Disease States

TL;DR: All intracellular proteins and many extracellular proteins are continually “turning over;” i.e. they are being hydrolyzed to their constituent amino acids and replaced by new synthesis.
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