scholarly journals Chronic Alcohol Consumption Enhances Skeletal Muscle Wasting in Mice Bearing Cachectic Cancers: The Role of TNFα/Myostatin Axis

2019 ◽  
Vol 44 (1) ◽  
pp. 66-77 ◽  
Author(s):  
Yuanfei Li ◽  
Faya Zhang ◽  
Samantha Modrak ◽  
Alex Little ◽  
Hui Zhang
Keyword(s):  
Skeletal Muscle ◽  
Alcohol Consumption ◽  
Muscle Wasting ◽  
Chronic Alcohol ◽  
Chronic Alcohol Consumption ◽  
Skeletal Muscle Wasting

Temporal effect of alcohol consumption on reactivity of pial arterioles: role of oxygen radicals

2001 ◽  
Vol 280 (3) ◽  
pp. H992-H1001 ◽  
Author(s):  
Hong Sun ◽  
William G. Mayhan
Keyword(s):  
Nitric Oxide ◽  
Free Radicals ◽  
Alcohol Consumption ◽  
Nitric Oxide Synthase ◽  
Chronic Alcohol ◽  
Chronic Alcohol Consumption ◽  
Oxygen Derived Free Radicals ◽  
Pial Arterioles ◽  
Oxide Synthase

Chronic alcohol consumption reduces nitric oxide synthase-dependent responses of pial arterioles via mechanisms that remain uncertain. In addition, the temporal effects of alcohol on pial arterioles is unclear. Thus our goals were to examine the role of oxygen-derived free radicals in alcohol-induced impairment of cerebrovascular reactivity and the temporal effect of alcohol on reactivity of pial arterioles. Sprague-Dawley rats were pair-fed a liquid diet with or without alcohol for 2–3 wk, 2–3 mo, or 5–6 mo. We measured the in vivo diameter of pial arterioles in response to nitric oxide synthase-dependent dilators acetylcholine and ADP and the nitric oxide synthase-independent dilator nitroglycerin. In nonalcohol-fed rats, acetylcholine (1.0 and 10 μM) and ADP (10 and 100 μM) produced dose-related dilatation of pial arterioles. Whereas there was no difference in reactivity of arterioles to the agonists in rats fed the nonalcohol and alcohol diets for a period of 2–3 wk, there was a significant impairment in reactivity of arterioles to acetylcholine and ADP, but not nitroglycerin, in rats fed the alcohol diet for longer durations. We then found that treatment with superoxide dismutase did not alter baseline diameter of pial arterioles in nonalcohol-fed or alcohol-fed rats, but significantly improved impaired nitric oxide synthase-dependent dilatation of pial arterioles in alcohol-fed rats. Thus our findings suggest a temporal relationship in the effects of alcohol on reactivity of pial arterioles and that impaired nitric oxide synthase-dependent cerebral vasodilatation during chronic alcohol consumption may be related, in part, to enhanced release of oxygen-derived free radicals.

Role of exosomal microRNA in driving skeletal muscle wasting in COPD

2015 ◽  
Author(s):  
Hannah Burke ◽  
C. Mirella Spalluto ◽  
Doriana Cellura ◽  
Karl J. Staples ◽  
Tom M.A. Wilkinson
Keyword(s):  
Skeletal Muscle ◽  
Muscle Wasting ◽  
Skeletal Muscle Wasting ◽  
Exosomal Microrna

Cancer-Induced Fatigue and Skeletal Muscle Wasting: The Role of Exercise

2001 ◽  
Vol 2 (3) ◽  
pp. 186-197 ◽  
Author(s):  
Sadeeka Al-Majid ◽  
Donna O. McCarthy
Keyword(s):  
Skeletal Muscle ◽  
Resistance Exercise ◽  
Muscle Wasting ◽  
Activity Level ◽  
Future Research ◽  
Physiological Mechanisms ◽  
Cancer Related Fatigue ◽  
Skeletal Muscle Wasting ◽  
Clinical Conditions

Fatigue is the most frequently reported symptom by cancer patients. Many of these patients perceive fatigue as the most distressing symptom associated with their illness because it imposes limitations on their physical activity level. Skeletal muscle wasting, which occurs as part of cancer cachexia, is one of the mechanisms that contribute to fatigue. Cancerinduced skeletal muscle wasting may occur despite normal food intake and is not prevented by nutritional supplementation. Evidence suggests that endurance exercise ameliorates cancer-related fatigue. There is no compelling evidence to support that exerciseinduced reduction in fatigue is related to preservation of muscle mass. Resistance exercise attenuates muscle wasting associated with a variety of catabolic conditions. However, its effects on cancer-induced muscle wasting have not been adequately studied. This article describes the physiological mechanisms implicated in the induction of cancer-related muscle wasting, summarizes findings from endurance and resistance exercise studies in relation to fatigue and muscle wasting during cancer and selected clinical conditions, and proposes directions for future research.

scholarly journals Walk the Line: The Role of Ubiquitin in Regulating Transcription in Myocytes

Physiology ◽  
2019 ◽  
Vol 34 (5) ◽  
pp. 327-340 ◽  
Author(s):  
Vidyani Suryadevara ◽  
Monte S. Willis
Keyword(s):  
Skeletal Muscle ◽  
Quality Control ◽  
Transcription Factors ◽  
Muscle Wasting ◽  
Protein Quality ◽  
Skeletal Muscle Wasting ◽  
Ubiquitin Proteasome ◽  
Specific Activities ◽  
Novel Targets

The ubiquitin-proteasome offers novel targets for potential therapies with their specific activities and tissue localization. Recently, the expansion of our understanding of how ubiquitin ligases (E3s) specifically regulate transcription has demonstrated their roles in skeletal muscle, complementing their roles in protein quality control and protein degradation. This review focuses on skeletal muscle E3s that regulate transcription factors critical to myogenesis and the maintenance of skeletal muscle wasting diseases.

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