Skeletal Muscle Abnormalities in Heart Failure

Kinugawa, Shintaro; Takada, Shingo; Matsushima, Shouji; Okita, Koichi; Tsutsui, Hiroyuki

doi:10.1536/ihj.15-108

Cited by 101 publications

(44 citation statements)

References 136 publications

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“…With respect to skeletal muscle, a variety of alterations specific to muscle structure and metabolic state, including muscle atrophy, alterations in fiber type, reduced mitochondrial enzymes, and decreased mitochondrial volume density, have all been associated with HFrEF [36–39]. Though an in-depth discussion of these skeletal muscle maladaptations in HFrEF is beyond the scope of the present discussion, this topic has been the subject of several recent reviews [40–42]. The skeletal muscle vasculature also appears to be altered as a consequence of the disease.…”

Section: Vascular Function In Hfrefmentioning

confidence: 99%

Peripheral vascular function, oxygen delivery and utilization: the impact of oxidative stress in aging and heart failure with reduced ejection fraction

2016

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The aging process appears to be a precursor to many age-related diseases, perhaps the most impactful of which is cardiovascular disease (CVD). Heart disease, a manifestation of CVD, is the leading cause of death in the USA, and heart failure (HF), a syndrome that develops as a consequence of heart disease, now affects almost six million American. Importantly, as this is an age-related disease, this number is likely to grow along with the ever-increasing elderly population. Hallmarks of the aging process and HF patients with a reduced ejection fraction (HFrEF) include exercise intolerance, premature fatigue, and limited oxygen delivery and utilization, perhaps as a consequence of diminished peripheral vascular function. Free radicals and oxidative stress have been implicated in this peripheral vascular dysfunction, as a redox imbalance may directly impact the function of the vascular endothelium. This review aims to bring together studies that have examined the impact of oxidative stress on peripheral vascular function and oxygen delivery and utilization with both healthy aging and HFrEF.

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Section: Vascular Function In Hfrefmentioning

confidence: 99%

Peripheral vascular function, oxygen delivery and utilization: the impact of oxidative stress in aging and heart failure with reduced ejection fraction

2016

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“…Impairment of muscle function can lead to many pathological changes including diabetes, obesity, and muscle wasting, as well as aging [3,4,5]. In vitro studies using muscle cells have been carried out as a means of predicting in vivo effects.…”

Section: Introductionmentioning

confidence: 99%

Electrical Impedance Monitoring of C2C12 Myoblast Differentiation on an Indium Tin Oxide Electrode

Ilhwan

Hong

Jun³

et al. 2016

Sensors

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Electrical cell-substrate impedance sensing is increasingly being used for label-free and real-time monitoring of changes in cell morphology and number during cell growth, drug screening, and differentiation. In this study, we evaluated the feasibility of using ECIS to monitor C2C12 myoblast differentiation using a fabricated indium tin oxide (ITO) electrode-based chip. C2C12 myoblast differentiation on the ITO electrode was validated based on decreases in the mRNA level of MyoD and increases in the mRNA levels of myogenin and myosin heavy chain (MHC). Additionally, MHC expression and morphological changes in myoblasts differentiated on the ITO electrode were comparable to those in cells in the control culture dish. From the monitoring the integration of the resistance change at 21.5 kHz, the cell differentiation was label-free and real-time detectable in 30 h of differentiation (p < 0.05).

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“…Moreover, this feature has been reported to be an independent predictor of mortality (Wei et al 2000). We previously reported that the reduced exercise capacity and impaired skeletal muscle mitochondrial function in mice with high-fat diet (HFD)-induced type 2 diabetes were due to enhanced oxidative stress via the activation of NAD(P)H oxidase (Yokota et al 2009;Takada et al 2013Takada et al , 2014Kinugawa et al 2015). Another study reported that NAD(P)H oxidase-induced superoxide anion (O 2 · − ) production was increased in the skeletal muscle of mice with insulin resistance-induced diabetes (Bonnard et al 2008).…”

Section: Introductionmentioning

confidence: 99%

Sesamin prevents decline in exercise capacity and impairment of skeletal muscle mitochondrial function in mice with high‐fat diet‐induced diabetes

Takada

Kinugawa

Matsushima

et al. 2015

Experimental Physiology

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New Findings What is the central question of this study? Our aim was to examine whether sesamin can prevent a decline in exercise capacity in high‐fat diet‐induced diabetic mice. Our hypothesis was that maintenance of mitochondrial function and attenuation of oxidative stress in the skeletal muscle would contribute to this result. What is the main finding and its importance? The new findings are that sesamin prevents the diabetes‐induced decrease in exercise capacity and impairment of mitochondrial function through the inhibition of NAD(P)H oxidase‐dependent oxidative stress in the skeletal muscle. Sesamin may be useful as a novel agent for the treatment of diabetes mellitus. AbstractWe previously reported that exercise capacity and skeletal muscle mitochondrial function in diabetic mice were impaired, in association with the activation of NAD(P)H oxidase. It has been reported that sesamin inhibits NAD(P)H oxidase‐induced superoxide production. Therefore, we examined whether the antioxidant sesamin could prevent a decline in exercise capacity in mice with high‐fat diet (HFD)‐induced diabetes. C57BL/6J mice were fed a normal diet (ND) or HFD, then treated or not with sesamin (0.2%) to yield the following four groups: ND, ND+Sesamin, HFD and HFD+Sesamin (n = 10 each). After 8 weeks, body weight, fat weight, blood glucose, insulin, triglyceride, total cholesterol and fatty acid were significantly increased in HFD compared with ND mice. Sesamin prevented the increases in blood insulin and lipid levels in HFD‐fed mice, but did not affect the plasma glucose. Exercise capacity determined by treadmill tests was significantly reduced in HFD mice, but almost completely recovered in HFD+Sesamin mice. Citrate synthase activity was significantly decreased in the skeletal muscle of HFD mice, and these decreases were also inhibited by sesamin. Superoxide anion and NAD(P)H oxidase activity were significantly increased in HFD mice compared with the ND mice and were ameliorated by sesamin. Sesamin prevented the decline in exercise capacity in HFD‐induced diabetic mice via maintenance of mitochondrial function, fat oxidation and attenuation of oxidative stress in the skeletal muscle. Our data suggest that sesamin may be useful as a novel agent for the treatment of diabetes mellitus.

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Skeletal Muscle Abnormalities in Heart Failure

Cited by 101 publications

References 136 publications

Peripheral vascular function, oxygen delivery and utilization: the impact of oxidative stress in aging and heart failure with reduced ejection fraction

Peripheral vascular function, oxygen delivery and utilization: the impact of oxidative stress in aging and heart failure with reduced ejection fraction

Electrical Impedance Monitoring of C2C12 Myoblast Differentiation on an Indium Tin Oxide Electrode

Sesamin prevents decline in exercise capacity and impairment of skeletal muscle mitochondrial function in mice with high‐fat diet‐induced diabetes

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