The Experts below are selected from a list of 11415 Experts worldwide ranked by ideXlab platform
Hisao Ogawa - One of the best experts on this subject based on the ideXlab platform.
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akt1 mediated fast glycolytic skeletal muscle growth attenuates renal damage in Experimental Kidney Disease
Journal of The American Society of Nephrology, 2014Co-Authors: Shinsuke Hanatani, Yasuhiro Izumiya, Satoshi Araki, Taku Rokutanda, Yuichi Kimura, Kenneth Walsh, Hisao OgawaAbstract:Muscle wasting is frequently observed in patients with Kidney Disease, and low muscle strength is associated with poor outcomes in these patients. However, little is known about the effects of skeletal muscle growth per se on Kidney Diseases. In this study, we utilized a skeletal muscle-specific, inducible Akt1 transgenic (Akt1 TG) mouse model that promotes the growth of functional skeletal muscle independent of exercise to investigate the effects of muscle growth on Kidney Diseases. Seven days after Akt1 activation in skeletal muscle, renal injury was induced by unilateral ureteral obstruction (UUO) in Akt1 TG and wild-type (WT) control mice. The expression of atrogin-1, an atrophy-inducing gene in skeletal muscle, was upregulated 7 days after UUO in WT mice but not in Akt1 TG mice. UUO-induced renal interstitial fibrosis, tubular injury, apoptosis, and increased expression of inflammatory, fibrosis-related, and adhesion molecule genes were significantly diminished in Akt1 TG mice compared with WT mice. An increase in the activating phosphorylation of eNOS in the Kidney accompanied the attenuation of renal damage by myogenic Akt1 activation. Treatment with the NOS inhibitor L-NAME abolished the protective effect of skeletal muscle Akt activation on obstructive Kidney Disease. In conclusion, Akt1-mediated muscle growth reduces renal damage in a model of obstructive Kidney Disease. This improvement appears to be mediated by an increase in eNOS signaling in the Kidney. Our data support the concept that loss of muscle mass during Kidney Disease can contribute to renal failure, and maintaining muscle mass may improve clinical outcome.
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abstract 11999 akt1 mediated fast glycolytic skeletal muscle growth reduces pathological renal damages in Experimental Kidney Disease
Circulation, 2013Co-Authors: Yasuhiro Izumiya, Shinsuke Hanatani, Satoshi Araki, Taku Rokutanda, Yuichi Kimura, Hisao OgawaAbstract:Introduction: Muscle wasting is frequently observed in patients with chronic Kidney Disease, and low muscle strength is associated with poor outcomes in these patients. Whereas, little is known about the clinical utility of increasing in skeletal muscle mass on Kidney Diseases. Hypothesis: Skeletal muscle growth attenuates pathological renal damages after mouse model of Kidney Diseases. Methods: We utilized skeletal muscle-specific, inducible Akt1 transgenic (Akt1 TG) mice, that can lead to the growth of functional skeletal muscle. Seven days after Akt1 activation in skeletal muscle, renal injury was induced by unilateral ureteral obstruction (UUO) in Akt1 TG and wild type (WT) control mice. Renal damages were evaluated by histological and gene expression analysis at 3, 7, and 14 days after UUO. Results: Activation of Akt1 signaling in myofibers led to an increase in skeletal muscle mass, assessed by gastrocnemius muscle weight at 7 days after surgery (171.8 vs. 256.7 mg; p≤0.001). Atrogin-1, atrophy-related gene, expression in skeletal muscle was robustly upregulated 7 days after UUO in WT mice but not in Akt1 TG mice, suggesting that muscle atrophy program was blocked by myogenic Akt1 activation. Masson’s trichrome and PAS stained histological sections revealed that renal interstitial fibrosis and tubular injury was dramatically increased by UUO in WT mice, but these changes were diminished in Akt1 TG mice. UUO-induced increase in inflammatory-related genes and adhesion molecule genes expression were significantly decreased in Akt1 TG mice compared to WT mice. Akt1-mediated skeletal muscle growth also attenuated fibrosis-related genes expression. Attenuated renal damages by myogenic Akt1 activation were accompanied by increasing endothelial nitric oxide synthase (eNOS) phosphorylation in Kidney tissue. The protective effect of skeletal muscle Akt activation on obstructive Kidney was abolished by treatment with the NOS inhibitor L-NAME. Conclusions: Akt1-mediated skeletal muscle growth reduces renal interstitial fibrosis and inflammation after UUO. This improvement appears to be mediated by eNOS-signaling in the Kidney. Our data suggest clinical utility of exercise lead to a skeletal muscle growth in patients with Kidney Diseases.
Yasuhiro Izumiya - One of the best experts on this subject based on the ideXlab platform.
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akt1 mediated fast glycolytic skeletal muscle growth attenuates renal damage in Experimental Kidney Disease
Journal of The American Society of Nephrology, 2014Co-Authors: Shinsuke Hanatani, Yasuhiro Izumiya, Satoshi Araki, Taku Rokutanda, Yuichi Kimura, Kenneth Walsh, Hisao OgawaAbstract:Muscle wasting is frequently observed in patients with Kidney Disease, and low muscle strength is associated with poor outcomes in these patients. However, little is known about the effects of skeletal muscle growth per se on Kidney Diseases. In this study, we utilized a skeletal muscle-specific, inducible Akt1 transgenic (Akt1 TG) mouse model that promotes the growth of functional skeletal muscle independent of exercise to investigate the effects of muscle growth on Kidney Diseases. Seven days after Akt1 activation in skeletal muscle, renal injury was induced by unilateral ureteral obstruction (UUO) in Akt1 TG and wild-type (WT) control mice. The expression of atrogin-1, an atrophy-inducing gene in skeletal muscle, was upregulated 7 days after UUO in WT mice but not in Akt1 TG mice. UUO-induced renal interstitial fibrosis, tubular injury, apoptosis, and increased expression of inflammatory, fibrosis-related, and adhesion molecule genes were significantly diminished in Akt1 TG mice compared with WT mice. An increase in the activating phosphorylation of eNOS in the Kidney accompanied the attenuation of renal damage by myogenic Akt1 activation. Treatment with the NOS inhibitor L-NAME abolished the protective effect of skeletal muscle Akt activation on obstructive Kidney Disease. In conclusion, Akt1-mediated muscle growth reduces renal damage in a model of obstructive Kidney Disease. This improvement appears to be mediated by an increase in eNOS signaling in the Kidney. Our data support the concept that loss of muscle mass during Kidney Disease can contribute to renal failure, and maintaining muscle mass may improve clinical outcome.
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abstract 11999 akt1 mediated fast glycolytic skeletal muscle growth reduces pathological renal damages in Experimental Kidney Disease
Circulation, 2013Co-Authors: Yasuhiro Izumiya, Shinsuke Hanatani, Satoshi Araki, Taku Rokutanda, Yuichi Kimura, Hisao OgawaAbstract:Introduction: Muscle wasting is frequently observed in patients with chronic Kidney Disease, and low muscle strength is associated with poor outcomes in these patients. Whereas, little is known about the clinical utility of increasing in skeletal muscle mass on Kidney Diseases. Hypothesis: Skeletal muscle growth attenuates pathological renal damages after mouse model of Kidney Diseases. Methods: We utilized skeletal muscle-specific, inducible Akt1 transgenic (Akt1 TG) mice, that can lead to the growth of functional skeletal muscle. Seven days after Akt1 activation in skeletal muscle, renal injury was induced by unilateral ureteral obstruction (UUO) in Akt1 TG and wild type (WT) control mice. Renal damages were evaluated by histological and gene expression analysis at 3, 7, and 14 days after UUO. Results: Activation of Akt1 signaling in myofibers led to an increase in skeletal muscle mass, assessed by gastrocnemius muscle weight at 7 days after surgery (171.8 vs. 256.7 mg; p≤0.001). Atrogin-1, atrophy-related gene, expression in skeletal muscle was robustly upregulated 7 days after UUO in WT mice but not in Akt1 TG mice, suggesting that muscle atrophy program was blocked by myogenic Akt1 activation. Masson’s trichrome and PAS stained histological sections revealed that renal interstitial fibrosis and tubular injury was dramatically increased by UUO in WT mice, but these changes were diminished in Akt1 TG mice. UUO-induced increase in inflammatory-related genes and adhesion molecule genes expression were significantly decreased in Akt1 TG mice compared to WT mice. Akt1-mediated skeletal muscle growth also attenuated fibrosis-related genes expression. Attenuated renal damages by myogenic Akt1 activation were accompanied by increasing endothelial nitric oxide synthase (eNOS) phosphorylation in Kidney tissue. The protective effect of skeletal muscle Akt activation on obstructive Kidney was abolished by treatment with the NOS inhibitor L-NAME. Conclusions: Akt1-mediated skeletal muscle growth reduces renal interstitial fibrosis and inflammation after UUO. This improvement appears to be mediated by eNOS-signaling in the Kidney. Our data suggest clinical utility of exercise lead to a skeletal muscle growth in patients with Kidney Diseases.
Shinsuke Hanatani - One of the best experts on this subject based on the ideXlab platform.
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akt1 mediated fast glycolytic skeletal muscle growth attenuates renal damage in Experimental Kidney Disease
Journal of The American Society of Nephrology, 2014Co-Authors: Shinsuke Hanatani, Yasuhiro Izumiya, Satoshi Araki, Taku Rokutanda, Yuichi Kimura, Kenneth Walsh, Hisao OgawaAbstract:Muscle wasting is frequently observed in patients with Kidney Disease, and low muscle strength is associated with poor outcomes in these patients. However, little is known about the effects of skeletal muscle growth per se on Kidney Diseases. In this study, we utilized a skeletal muscle-specific, inducible Akt1 transgenic (Akt1 TG) mouse model that promotes the growth of functional skeletal muscle independent of exercise to investigate the effects of muscle growth on Kidney Diseases. Seven days after Akt1 activation in skeletal muscle, renal injury was induced by unilateral ureteral obstruction (UUO) in Akt1 TG and wild-type (WT) control mice. The expression of atrogin-1, an atrophy-inducing gene in skeletal muscle, was upregulated 7 days after UUO in WT mice but not in Akt1 TG mice. UUO-induced renal interstitial fibrosis, tubular injury, apoptosis, and increased expression of inflammatory, fibrosis-related, and adhesion molecule genes were significantly diminished in Akt1 TG mice compared with WT mice. An increase in the activating phosphorylation of eNOS in the Kidney accompanied the attenuation of renal damage by myogenic Akt1 activation. Treatment with the NOS inhibitor L-NAME abolished the protective effect of skeletal muscle Akt activation on obstructive Kidney Disease. In conclusion, Akt1-mediated muscle growth reduces renal damage in a model of obstructive Kidney Disease. This improvement appears to be mediated by an increase in eNOS signaling in the Kidney. Our data support the concept that loss of muscle mass during Kidney Disease can contribute to renal failure, and maintaining muscle mass may improve clinical outcome.
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abstract 11999 akt1 mediated fast glycolytic skeletal muscle growth reduces pathological renal damages in Experimental Kidney Disease
Circulation, 2013Co-Authors: Yasuhiro Izumiya, Shinsuke Hanatani, Satoshi Araki, Taku Rokutanda, Yuichi Kimura, Hisao OgawaAbstract:Introduction: Muscle wasting is frequently observed in patients with chronic Kidney Disease, and low muscle strength is associated with poor outcomes in these patients. Whereas, little is known about the clinical utility of increasing in skeletal muscle mass on Kidney Diseases. Hypothesis: Skeletal muscle growth attenuates pathological renal damages after mouse model of Kidney Diseases. Methods: We utilized skeletal muscle-specific, inducible Akt1 transgenic (Akt1 TG) mice, that can lead to the growth of functional skeletal muscle. Seven days after Akt1 activation in skeletal muscle, renal injury was induced by unilateral ureteral obstruction (UUO) in Akt1 TG and wild type (WT) control mice. Renal damages were evaluated by histological and gene expression analysis at 3, 7, and 14 days after UUO. Results: Activation of Akt1 signaling in myofibers led to an increase in skeletal muscle mass, assessed by gastrocnemius muscle weight at 7 days after surgery (171.8 vs. 256.7 mg; p≤0.001). Atrogin-1, atrophy-related gene, expression in skeletal muscle was robustly upregulated 7 days after UUO in WT mice but not in Akt1 TG mice, suggesting that muscle atrophy program was blocked by myogenic Akt1 activation. Masson’s trichrome and PAS stained histological sections revealed that renal interstitial fibrosis and tubular injury was dramatically increased by UUO in WT mice, but these changes were diminished in Akt1 TG mice. UUO-induced increase in inflammatory-related genes and adhesion molecule genes expression were significantly decreased in Akt1 TG mice compared to WT mice. Akt1-mediated skeletal muscle growth also attenuated fibrosis-related genes expression. Attenuated renal damages by myogenic Akt1 activation were accompanied by increasing endothelial nitric oxide synthase (eNOS) phosphorylation in Kidney tissue. The protective effect of skeletal muscle Akt activation on obstructive Kidney was abolished by treatment with the NOS inhibitor L-NAME. Conclusions: Akt1-mediated skeletal muscle growth reduces renal interstitial fibrosis and inflammation after UUO. This improvement appears to be mediated by eNOS-signaling in the Kidney. Our data suggest clinical utility of exercise lead to a skeletal muscle growth in patients with Kidney Diseases.
Yuichi Kimura - One of the best experts on this subject based on the ideXlab platform.
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akt1 mediated fast glycolytic skeletal muscle growth attenuates renal damage in Experimental Kidney Disease
Journal of The American Society of Nephrology, 2014Co-Authors: Shinsuke Hanatani, Yasuhiro Izumiya, Satoshi Araki, Taku Rokutanda, Yuichi Kimura, Kenneth Walsh, Hisao OgawaAbstract:Muscle wasting is frequently observed in patients with Kidney Disease, and low muscle strength is associated with poor outcomes in these patients. However, little is known about the effects of skeletal muscle growth per se on Kidney Diseases. In this study, we utilized a skeletal muscle-specific, inducible Akt1 transgenic (Akt1 TG) mouse model that promotes the growth of functional skeletal muscle independent of exercise to investigate the effects of muscle growth on Kidney Diseases. Seven days after Akt1 activation in skeletal muscle, renal injury was induced by unilateral ureteral obstruction (UUO) in Akt1 TG and wild-type (WT) control mice. The expression of atrogin-1, an atrophy-inducing gene in skeletal muscle, was upregulated 7 days after UUO in WT mice but not in Akt1 TG mice. UUO-induced renal interstitial fibrosis, tubular injury, apoptosis, and increased expression of inflammatory, fibrosis-related, and adhesion molecule genes were significantly diminished in Akt1 TG mice compared with WT mice. An increase in the activating phosphorylation of eNOS in the Kidney accompanied the attenuation of renal damage by myogenic Akt1 activation. Treatment with the NOS inhibitor L-NAME abolished the protective effect of skeletal muscle Akt activation on obstructive Kidney Disease. In conclusion, Akt1-mediated muscle growth reduces renal damage in a model of obstructive Kidney Disease. This improvement appears to be mediated by an increase in eNOS signaling in the Kidney. Our data support the concept that loss of muscle mass during Kidney Disease can contribute to renal failure, and maintaining muscle mass may improve clinical outcome.
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abstract 11999 akt1 mediated fast glycolytic skeletal muscle growth reduces pathological renal damages in Experimental Kidney Disease
Circulation, 2013Co-Authors: Yasuhiro Izumiya, Shinsuke Hanatani, Satoshi Araki, Taku Rokutanda, Yuichi Kimura, Hisao OgawaAbstract:Introduction: Muscle wasting is frequently observed in patients with chronic Kidney Disease, and low muscle strength is associated with poor outcomes in these patients. Whereas, little is known about the clinical utility of increasing in skeletal muscle mass on Kidney Diseases. Hypothesis: Skeletal muscle growth attenuates pathological renal damages after mouse model of Kidney Diseases. Methods: We utilized skeletal muscle-specific, inducible Akt1 transgenic (Akt1 TG) mice, that can lead to the growth of functional skeletal muscle. Seven days after Akt1 activation in skeletal muscle, renal injury was induced by unilateral ureteral obstruction (UUO) in Akt1 TG and wild type (WT) control mice. Renal damages were evaluated by histological and gene expression analysis at 3, 7, and 14 days after UUO. Results: Activation of Akt1 signaling in myofibers led to an increase in skeletal muscle mass, assessed by gastrocnemius muscle weight at 7 days after surgery (171.8 vs. 256.7 mg; p≤0.001). Atrogin-1, atrophy-related gene, expression in skeletal muscle was robustly upregulated 7 days after UUO in WT mice but not in Akt1 TG mice, suggesting that muscle atrophy program was blocked by myogenic Akt1 activation. Masson’s trichrome and PAS stained histological sections revealed that renal interstitial fibrosis and tubular injury was dramatically increased by UUO in WT mice, but these changes were diminished in Akt1 TG mice. UUO-induced increase in inflammatory-related genes and adhesion molecule genes expression were significantly decreased in Akt1 TG mice compared to WT mice. Akt1-mediated skeletal muscle growth also attenuated fibrosis-related genes expression. Attenuated renal damages by myogenic Akt1 activation were accompanied by increasing endothelial nitric oxide synthase (eNOS) phosphorylation in Kidney tissue. The protective effect of skeletal muscle Akt activation on obstructive Kidney was abolished by treatment with the NOS inhibitor L-NAME. Conclusions: Akt1-mediated skeletal muscle growth reduces renal interstitial fibrosis and inflammation after UUO. This improvement appears to be mediated by eNOS-signaling in the Kidney. Our data suggest clinical utility of exercise lead to a skeletal muscle growth in patients with Kidney Diseases.
Taku Rokutanda - One of the best experts on this subject based on the ideXlab platform.
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akt1 mediated fast glycolytic skeletal muscle growth attenuates renal damage in Experimental Kidney Disease
Journal of The American Society of Nephrology, 2014Co-Authors: Shinsuke Hanatani, Yasuhiro Izumiya, Satoshi Araki, Taku Rokutanda, Yuichi Kimura, Kenneth Walsh, Hisao OgawaAbstract:Muscle wasting is frequently observed in patients with Kidney Disease, and low muscle strength is associated with poor outcomes in these patients. However, little is known about the effects of skeletal muscle growth per se on Kidney Diseases. In this study, we utilized a skeletal muscle-specific, inducible Akt1 transgenic (Akt1 TG) mouse model that promotes the growth of functional skeletal muscle independent of exercise to investigate the effects of muscle growth on Kidney Diseases. Seven days after Akt1 activation in skeletal muscle, renal injury was induced by unilateral ureteral obstruction (UUO) in Akt1 TG and wild-type (WT) control mice. The expression of atrogin-1, an atrophy-inducing gene in skeletal muscle, was upregulated 7 days after UUO in WT mice but not in Akt1 TG mice. UUO-induced renal interstitial fibrosis, tubular injury, apoptosis, and increased expression of inflammatory, fibrosis-related, and adhesion molecule genes were significantly diminished in Akt1 TG mice compared with WT mice. An increase in the activating phosphorylation of eNOS in the Kidney accompanied the attenuation of renal damage by myogenic Akt1 activation. Treatment with the NOS inhibitor L-NAME abolished the protective effect of skeletal muscle Akt activation on obstructive Kidney Disease. In conclusion, Akt1-mediated muscle growth reduces renal damage in a model of obstructive Kidney Disease. This improvement appears to be mediated by an increase in eNOS signaling in the Kidney. Our data support the concept that loss of muscle mass during Kidney Disease can contribute to renal failure, and maintaining muscle mass may improve clinical outcome.
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abstract 11999 akt1 mediated fast glycolytic skeletal muscle growth reduces pathological renal damages in Experimental Kidney Disease
Circulation, 2013Co-Authors: Yasuhiro Izumiya, Shinsuke Hanatani, Satoshi Araki, Taku Rokutanda, Yuichi Kimura, Hisao OgawaAbstract:Introduction: Muscle wasting is frequently observed in patients with chronic Kidney Disease, and low muscle strength is associated with poor outcomes in these patients. Whereas, little is known about the clinical utility of increasing in skeletal muscle mass on Kidney Diseases. Hypothesis: Skeletal muscle growth attenuates pathological renal damages after mouse model of Kidney Diseases. Methods: We utilized skeletal muscle-specific, inducible Akt1 transgenic (Akt1 TG) mice, that can lead to the growth of functional skeletal muscle. Seven days after Akt1 activation in skeletal muscle, renal injury was induced by unilateral ureteral obstruction (UUO) in Akt1 TG and wild type (WT) control mice. Renal damages were evaluated by histological and gene expression analysis at 3, 7, and 14 days after UUO. Results: Activation of Akt1 signaling in myofibers led to an increase in skeletal muscle mass, assessed by gastrocnemius muscle weight at 7 days after surgery (171.8 vs. 256.7 mg; p≤0.001). Atrogin-1, atrophy-related gene, expression in skeletal muscle was robustly upregulated 7 days after UUO in WT mice but not in Akt1 TG mice, suggesting that muscle atrophy program was blocked by myogenic Akt1 activation. Masson’s trichrome and PAS stained histological sections revealed that renal interstitial fibrosis and tubular injury was dramatically increased by UUO in WT mice, but these changes were diminished in Akt1 TG mice. UUO-induced increase in inflammatory-related genes and adhesion molecule genes expression were significantly decreased in Akt1 TG mice compared to WT mice. Akt1-mediated skeletal muscle growth also attenuated fibrosis-related genes expression. Attenuated renal damages by myogenic Akt1 activation were accompanied by increasing endothelial nitric oxide synthase (eNOS) phosphorylation in Kidney tissue. The protective effect of skeletal muscle Akt activation on obstructive Kidney was abolished by treatment with the NOS inhibitor L-NAME. Conclusions: Akt1-mediated skeletal muscle growth reduces renal interstitial fibrosis and inflammation after UUO. This improvement appears to be mediated by eNOS-signaling in the Kidney. Our data suggest clinical utility of exercise lead to a skeletal muscle growth in patients with Kidney Diseases.
