Zhaoyong Hu

Summary

Affiliation: Baylor College of Medicine
Country: USA

Publications

  1. ncbi Cellular signals activating muscle proteolysis in chronic kidney disease: a two-stage process
    Jie Du
    Nephrology Division, Baylor College of Medicine, One Baylor Plaza-BCM 285, Houston, TX 77030, USA
    Int J Biochem Cell Biol 37:2147-55. 2005
  2. ncbi PTEN expression contributes to the regulation of muscle protein degradation in diabetes
    Zhaoyong Hu
    Baylor College of Medicine, Nephrology Division, M S BCM 285, One Baylor Plaza, Alkek N 520, Houston, TX 77030, USA
    Diabetes 56:2449-56. 2007
  3. ncbi PTEN inhibition improves muscle regeneration in mice fed a high-fat diet
    Zhaoyong Hu
    Nephrology Division, Baylor College of Medicine, Houston, Texas, USA
    Diabetes 59:1312-20. 2010
  4. ncbi Endogenous glucocorticoids and impaired insulin signaling are both required to stimulate muscle wasting under pathophysiological conditions in mice
    Zhaoyong Hu
    Nephrology Division, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA
    J Clin Invest 119:3059-69. 2009
  5. ncbi Development of a diagnostic method for detecting increased muscle protein degradation in patients with catabolic conditions
    Biruh T Workeneh
    Medicine and Surgery, University of Texas Medical Branch, Galveston, Texas, USA
    J Am Soc Nephrol 17:3233-9. 2006
  6. ncbi IL-6 and serum amyloid A synergy mediates angiotensin II-induced muscle wasting
    Liping Zhang
    Nephrology Division, Baylor College of Medicine, Houston, TX 77030, USA
    J Am Soc Nephrol 20:604-12. 2009
  7. ncbi Pharmacological inhibition of myostatin suppresses systemic inflammation and muscle atrophy in mice with chronic kidney disease
    Liping Zhang
    Nephrology Division, Baylor College of Medicine, Houston, Texas, USA 77030, USA
    FASEB J 25:1653-63. 2011
  8. ncbi Regulation of muscle protein degradation: coordinated control of apoptotic and ubiquitin-proteasome systems by phosphatidylinositol 3 kinase
    Seoung Woo Lee
    Nephrology Division, Department of Medicine, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555, USA
    J Am Soc Nephrol 15:1537-45. 2004
  9. ncbi Ghrelin treatment of chronic kidney disease: improvements in lean body mass and cytokine profile
    Mark D DeBoer
    Department of Pediatrics, University of Virginia, Charlottesville, VA 22908, USA
    Endocrinology 149:827-35. 2008
  10. ncbi Insulin resistance accelerates muscle protein degradation: Activation of the ubiquitin-proteasome pathway by defects in muscle cell signaling
    Xiaonan Wang
    Renal Division, WMB 338, Emory University School of Medicine, M S 1930 001 1AG, 1639 Pierce Drive, Atlanta, Georgia 30322, USA
    Endocrinology 147:4160-8. 2006

Collaborators

Detail Information

Publications12

  1. ncbi Cellular signals activating muscle proteolysis in chronic kidney disease: a two-stage process
    Jie Du
    Nephrology Division, Baylor College of Medicine, One Baylor Plaza-BCM 285, Houston, TX 77030, USA
    Int J Biochem Cell Biol 37:2147-55. 2005
    ..Additional investigations will be needed to define the cell signaling processes that activate muscle proteolysis in uremia and catabolic conditions...
  2. ncbi PTEN expression contributes to the regulation of muscle protein degradation in diabetes
    Zhaoyong Hu
    Baylor College of Medicine, Nephrology Division, M S BCM 285, One Baylor Plaza, Alkek N 520, Houston, TX 77030, USA
    Diabetes 56:2449-56. 2007
    ..We evaluated the control of muscle protein synthesis and degradation in mouse models of type 1 and 2 diabetes to determine whether defects besides PI3K/Akt activities affect muscle metabolism...
  3. ncbi PTEN inhibition improves muscle regeneration in mice fed a high-fat diet
    Zhaoyong Hu
    Nephrology Division, Baylor College of Medicine, Houston, Texas, USA
    Diabetes 59:1312-20. 2010
    ..We also examined the regulation of phosphatidylinositol 3,4,5-trisphosphate (PIP(3)) during muscle regeneration because augmented IGF-1 signaling can improve muscle regeneration...
  4. ncbi Endogenous glucocorticoids and impaired insulin signaling are both required to stimulate muscle wasting under pathophysiological conditions in mice
    Zhaoyong Hu
    Nephrology Division, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA
    J Clin Invest 119:3059-69. 2009
    ..This nongenomic influence of the GR contributes to activation of muscle protein degradation. We therefore conclude that stimulation of muscle proteolysis requires 2 events, increased glucocorticoid levels and impaired insulin signaling...
  5. ncbi Development of a diagnostic method for detecting increased muscle protein degradation in patients with catabolic conditions
    Biruh T Workeneh
    Medicine and Surgery, University of Texas Medical Branch, Galveston, Texas, USA
    J Am Soc Nephrol 17:3233-9. 2006
    ....
  6. ncbi IL-6 and serum amyloid A synergy mediates angiotensin II-induced muscle wasting
    Liping Zhang
    Nephrology Division, Baylor College of Medicine, Houston, TX 77030, USA
    J Am Soc Nephrol 20:604-12. 2009
    ..Targeting the high levels of IL-6 and SAA in catabolic disorders might be a therapeutic approach to prevent muscle wasting...
  7. ncbi Pharmacological inhibition of myostatin suppresses systemic inflammation and muscle atrophy in mice with chronic kidney disease
    Liping Zhang
    Nephrology Division, Baylor College of Medicine, Houston, Texas, USA 77030, USA
    FASEB J 25:1653-63. 2011
    ..Myostatin antagonism might become a therapeutic strategy for improving muscle growth in CKD and other conditions with similar characteristics...
  8. ncbi Regulation of muscle protein degradation: coordinated control of apoptotic and ubiquitin-proteasome systems by phosphatidylinositol 3 kinase
    Seoung Woo Lee
    Nephrology Division, Department of Medicine, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555, USA
    J Am Soc Nephrol 15:1537-45. 2004
    ..When PI3K activity is low, both apoptotic and Ub-P'some pathways are activated coordinately to cause muscle proteolysis. This mechanism could increase muscle atrophy in conditions with impaired insulin responsiveness...
  9. ncbi Ghrelin treatment of chronic kidney disease: improvements in lean body mass and cytokine profile
    Mark D DeBoer
    Department of Pediatrics, University of Virginia, Charlottesville, VA 22908, USA
    Endocrinology 149:827-35. 2008
    ..We conclude that ghrelin treatment in uremia results in improved lean mass accrual in part due to suppressed muscle proteolysis and possibly related to antiinflammatory effects...
  10. ncbi Insulin resistance accelerates muscle protein degradation: Activation of the ubiquitin-proteasome pathway by defects in muscle cell signaling
    Xiaonan Wang
    Renal Division, WMB 338, Emory University School of Medicine, M S 1930 001 1AG, 1639 Pierce Drive, Atlanta, Georgia 30322, USA
    Endocrinology 147:4160-8. 2006
    ..Thus, insulin resistance causes muscle wasting by mechanisms that involve suppression of PI3K/Akt signaling leading to activation of caspase-3 and the ubiquitin-proteasome proteolytic pathway causing muscle protein degradation...
  11. ncbi Chronic kidney disease causes defects in signaling through the insulin receptor substrate/phosphatidylinositol 3-kinase/Akt pathway: implications for muscle atrophy
    James L Bailey
    Renal Division, Emory University School of Medicine, WMB 338, 1639 Pierce Drive, Atlanta, GA 30322, USA
    J Am Soc Nephrol 17:1388-94. 2006
    ..It is concluded that in CKD, acidosis and an increase in the PI3-K p85 subunit are mechanisms that contribute to suppression of PI3-K activity in muscle, and this leads to accelerated muscle proteolysis...
  12. ncbi Mitochondrial integrity and function in atherogenesis
    Scott W Ballinger
    Sealy Center for Molecular Cardiology and Division of Cardiology, The University of Texas Medical Branch, Galveston, Tex, USA
    Circulation 106:544-9. 2002
    ..CONCLUSIONS: Mitochondrial DNA damage may result from RS production in vascular tissues and may in turn be an early event in the initiation of atherosclerotic lesions...