Chang Seng Liang

Summary

Affiliation: University of Rochester
Country: USA

Publications

  1. ncbi request reprint Alterations by norepinephrine of cardiac sympathetic nerve terminal function and myocardial beta-adrenergic receptor sensitivity in the ferret: normalization by antioxidant vitamins
    C Liang
    Cardiology Unit, Department of Medicine, University of Rochester Medical Center, NY 14642 8679, USA
    Circulation 102:96-103. 2000
  2. ncbi request reprint Cardiac sympathetic neuroprotective effect of desipramine in tachycardia-induced cardiomyopathy
    Chang Seng Liang
    Department of Medicine, Cardiology Division, University of Rochester Medical Center, Box 679, 601 Elmwood Ave, Rochester, New York 14642, USA
    Am J Physiol Heart Circ Physiol 290:H995-1003. 2006
  3. ncbi request reprint Desipramine attenuates loss of cardiac sympathetic neurotransmitters produced by congestive heart failure and NE infusion
    Chang Seng Liang
    Cardiology Unit, Department of Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Am J Physiol Heart Circ Physiol 284:H1729-36. 2003
  4. ncbi request reprint Differential pre- and postsynaptic effects of desipramine on cardiac sympathetic nerve terminals in RHF
    Chang Seng Liang
    Cardiology Unit, Department of Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Am J Physiol Heart Circ Physiol 283:H1863-72. 2002
  5. ncbi request reprint Cardiac sympathetic nerve terminal function in congestive heart failure
    Chang Seng Liang
    School of Medicine and Dentistry, University of Rochester, Rochester, NY 14642, USA
    Acta Pharmacol Sin 28:921-7. 2007
  6. ncbi request reprint Cardiomyocyte apoptosis in autoimmune cardiomyopathy: mediated via endoplasmic reticulum stress and exaggerated by norepinephrine
    Weike Mao
    University of Rochester Medical Center, Department of Medicine, Cardiology Division, Box 679, 601 Elmwood Ave, Rochester, NY 14642, USA
    Am J Physiol Heart Circ Physiol 293:H1636-45. 2007
  7. ncbi request reprint Antioxidants attenuate myocyte apoptosis and improve cardiac function in CHF: association with changes in MAPK pathways
    Fuzhong Qin
    Cardiology Unit, Department of Medicine, University of Rochester Medical Center, Box 679, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Am J Physiol Heart Circ Physiol 285:H822-32. 2003
  8. ncbi request reprint Importance of antioxidant and antiapoptotic effects of beta-receptor blockers in heart failure therapy
    Keisuke Kawai
    Cardiology Unit, Department of Medicine, University of Rochester Medical Center, Rochester, New York 14642, USA
    Am J Physiol Heart Circ Physiol 287:H1003-12. 2004
  9. ncbi request reprint Extracellular norepinephrine reduces neuronal uptake of norepinephrine by oxidative stress in PC12 cells
    Weike Mao
    University of Rochester Medical Center, Cardiology Unit, Box 679, 601 Elmwood Ave, Rochester, NY 14642, USA
    Am J Physiol Heart Circ Physiol 287:H29-39. 2004
  10. pmc Adoptive passive transfer of rabbit beta1-adrenoceptor peptide immune cardiomyopathy into the Rag2-/- mouse: participation of the ER stress
    Jiahao Liu
    Cardiology Division, Department of Medicine, University of Rochester Medical Center, Rochester, New York 14642, USA
    J Mol Cell Cardiol 44:304-14. 2008

Research Grants

Collaborators

Detail Information

Publications22

  1. ncbi request reprint Alterations by norepinephrine of cardiac sympathetic nerve terminal function and myocardial beta-adrenergic receptor sensitivity in the ferret: normalization by antioxidant vitamins
    C Liang
    Cardiology Unit, Department of Medicine, University of Rochester Medical Center, NY 14642 8679, USA
    Circulation 102:96-103. 2000
    ..The present study was carried out to determine whether these changes could be prevented by antioxidants...
  2. ncbi request reprint Cardiac sympathetic neuroprotective effect of desipramine in tachycardia-induced cardiomyopathy
    Chang Seng Liang
    Department of Medicine, Cardiology Division, University of Rochester Medical Center, Box 679, 601 Elmwood Ave, Rochester, New York 14642, USA
    Am J Physiol Heart Circ Physiol 290:H995-1003. 2006
    ..Also, normal neuronal uptake of NE is required for NE or its oxidized metabolites to exert their neurotoxic effects...
  3. ncbi request reprint Desipramine attenuates loss of cardiac sympathetic neurotransmitters produced by congestive heart failure and NE infusion
    Chang Seng Liang
    Cardiology Unit, Department of Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Am J Physiol Heart Circ Physiol 284:H1729-36. 2003
    ..In addition, it shows that the anatomic integrity of the sympathetic nerves is relatively intact and that the neuronal damaging effect of NE involves the uptake of NE or its metabolites into the sympathetic nerves...
  4. ncbi request reprint Differential pre- and postsynaptic effects of desipramine on cardiac sympathetic nerve terminals in RHF
    Chang Seng Liang
    Cardiology Unit, Department of Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Am J Physiol Heart Circ Physiol 283:H1863-72. 2002
    ....
  5. ncbi request reprint Cardiac sympathetic nerve terminal function in congestive heart failure
    Chang Seng Liang
    School of Medicine and Dentistry, University of Rochester, Rochester, NY 14642, USA
    Acta Pharmacol Sin 28:921-7. 2007
    ..Finally, increasing evidence suggests and further studies are needed to show that the cardiac sympathetic nerve terminal function may be a direct target for pharmacologic treatment of congestive heart failure...
  6. ncbi request reprint Cardiomyocyte apoptosis in autoimmune cardiomyopathy: mediated via endoplasmic reticulum stress and exaggerated by norepinephrine
    Weike Mao
    University of Rochester Medical Center, Department of Medicine, Cardiology Division, Box 679, 601 Elmwood Ave, Rochester, NY 14642, USA
    Am J Physiol Heart Circ Physiol 293:H1636-45. 2007
    ..Thus ER stress occurs in autoimmune cardiomyopathy induced by beta(1)-EC(II) peptide, and this is enhanced by increased NE and caused by activation of the beta(1)-adrenergic receptor-coupled CaMKII, p38 MAPK, and ATF6 pathway...
  7. ncbi request reprint Antioxidants attenuate myocyte apoptosis and improve cardiac function in CHF: association with changes in MAPK pathways
    Fuzhong Qin
    Cardiology Unit, Department of Medicine, University of Rochester Medical Center, Box 679, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Am J Physiol Heart Circ Physiol 285:H822-32. 2003
    ..Furthermore, because NE infusion produced changes of JNK, p-p38, and p-ERK similar to those in CHF, we conclude that NE may play an important role in the production of oxidative stress, MAPK activation, and myocyte apoptosis in CHF...
  8. ncbi request reprint Importance of antioxidant and antiapoptotic effects of beta-receptor blockers in heart failure therapy
    Keisuke Kawai
    Cardiology Unit, Department of Medicine, University of Rochester Medical Center, Rochester, New York 14642, USA
    Am J Physiol Heart Circ Physiol 287:H1003-12. 2004
    ..473, P = 0.0001). Thus our findings suggest antioxidant and antiapoptotic actions of carvedilol and metoprolol are important determinants of clinical beneficial effects of beta-receptors in the treatment of CHF...
  9. ncbi request reprint Extracellular norepinephrine reduces neuronal uptake of norepinephrine by oxidative stress in PC12 cells
    Weike Mao
    University of Rochester Medical Center, Cardiology Unit, Box 679, 601 Elmwood Ave, Rochester, NY 14642, USA
    Am J Physiol Heart Circ Physiol 287:H29-39. 2004
    ..Thus our results support a functional role of oxidative stress in mediating the neuronal NE uptake reducing effect of NE and that this effect of NE on NET is a posttranscriptional event...
  10. pmc Adoptive passive transfer of rabbit beta1-adrenoceptor peptide immune cardiomyopathy into the Rag2-/- mouse: participation of the ER stress
    Jiahao Liu
    Cardiology Division, Department of Medicine, University of Rochester Medical Center, Rochester, New York 14642, USA
    J Mol Cell Cardiol 44:304-14. 2008
    ..Thus, we conclude that ER stress plays an important role in cell death and cardiac dysfunction in beta(1)-EC(II) IgG cardiomyopathy, and the effects of beta(1)-EC(II) IgG are mediated via the beta(1)-adrenergic receptor...
  11. ncbi request reprint Selegiline attenuates cardiac oxidative stress and apoptosis in heart failure: association with improvement of cardiac function
    Fuzhong Qin
    Cardiology Unit, Department of Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Box 679, Rochester, NY 14642, USA
    Eur J Pharmacol 461:149-58. 2003
    ..The antioxidant antiapoptotic effects of selegiline are potentially beneficial in the improvement of cardiac function in chronic heart failure...
  12. ncbi request reprint Norepinephrine induces endoplasmic reticulum stress and downregulation of norepinephrine transporter density in PC12 cells via oxidative stress
    Weike Mao
    Cardiology Unit, Department of Medicine, University of Rochester Medical Center, Rochester, New York 14642, USA
    Am J Physiol Heart Circ Physiol 288:H2381-9. 2005
    ..Interventions involving the ER stress pathways may provide novel therapeutic strategies for the treatment of sympathetic dysfunction in heart failure...
  13. ncbi request reprint Norepinephrine-induced oxidative stress causes PC-12 cell apoptosis by both endoplasmic reticulum stress and mitochondrial intrinsic pathway: inhibition of phosphatidylinositol 3-kinase survival pathway
    Weike Mao
    Cardiology Division, University of Rochester Medical Center, Box 679, 601 Elmwood Ave, Rochester, NY 14642, USA
    Am J Physiol Cell Physiol 290:C1373-84. 2006
    ..These results indicate that NE induced cell apoptosis by both ER stress and a mitochondrial death pathway and that the effects of NE were mediated via oxidative stress and inhibition of the PI3-kinase/Akt survival pathway...
  14. ncbi request reprint Progressive left ventricular remodeling, myocyte apoptosis, and protein signaling cascades after myocardial infarction in rabbits
    Fuzhong Qin
    Cardiology Unit, Department of Medicine, University of Rochester Medical Center, NY 14642, USA
    Biochim Biophys Acta 1740:499-513. 2005
    ..These changes in the remote noninfarcted myocardium may contribute to LV remodeling and dysfunction after MI...
  15. doi request reprint Pro-apoptotic effects of anti-beta1-adrenergic receptor antibodies in cultured rat cardiomyocytes: actions on endoplasmic reticulum and the prosurvival PI3K-Akt pathway
    Chang Seng Liang
    Department of Medicine, Cardiology Division, University of Rochester Medical Center, Rochester, NY 14642, USA
    Autoimmunity 41:434-41. 2008
    ....
  16. pmc ERKs/p53 signal transduction pathway is involved in doxorubicin-induced apoptosis in H9c2 cells and cardiomyocytes
    Jiahao Liu
    Cardiology Division, Department of Medicine, University of Rochester Medical Center, Rochester, New York, USA
    Am J Physiol Heart Circ Physiol 295:H1956-65. 2008
    ..ERKs and p53 may be considered as novel therapeutic targets for the treatment of doxorubicin-induced cardiotoxicity...
  17. pmc Darbepoetin alfa exerts a cardioprotective effect in autoimmune cardiomyopathy via reduction of ER stress and activation of the PI3K/Akt and STAT3 pathways
    Weike Mao
    Cardiology Division, Department of Medicine, University of Rochester Medical Center, Rochester, New York 14642, USA
    J Mol Cell Cardiol 45:250-60. 2008
    ..Thus, we conclude that darbepoetin alfa improves cardiac function and prevents progression of dilated cardiomyopathy probably by activating the PI3K/Akt and STAT3 pathways and reducing ER stress...
  18. ncbi request reprint Loss of cardiac sympathetic neurotransmitters in heart failure and NE infusion is associated with reduced NGF
    Fuzhong Qin
    Department of Medicine, University of Rochester Medical Center, 601 Elmwood Ave, Rochester, NY 14642, USA
    Am J Physiol Heart Circ Physiol 282:H363-71. 2002
    ..Findings indicate that decrease of cardiac sympathetic transmitters in heart failure is associated with NE-mediated reduction of NGF and TrKA...
  19. ncbi request reprint Cardioselective overexpression of HO-1 prevents I/R-induced cardiac dysfunction and apoptosis
    Sreesatya Raju Vulapalli
    Cardiology Unit, Department of Medicine, University of Rochester School of Medicine, 601 Elmwood Avenue, Rochester, NY 14642, USA
    Am J Physiol Heart Circ Physiol 283:H688-94. 2002
    ..Our results indicate that cardioselective overexpression of HO-1 exerts a cardioprotective effect after myocardial I/R in mice, and this effect is probably mediated via an antiapoptotic action of HO-1...
  20. pmc Relationship of plasma galectin-3 to renal function in patients with heart failure: effects of clinical status, pathophysiology of heart failure, and presence or absence of heart failure
    Deepa M Gopal
    Cardiovascular Medicine Section, Department of Medicine, Myocardial Biology Unit, Boston University Medical Center, Boston, MA 02118, USA
    J Am Heart Assoc 1:e000760. 2012
    ..Plasma GAL-3 is inversely related to renal function. It is not known whether the relationship between renal function and GAL-3 is influenced by clinical decompensation, type of HF, or the presence or absence of clinical HF...
  21. ncbi request reprint Association of C-reactive protein and serum amyloid A with recurrent coronary events in stable patients after healing of acute myocardial infarction
    Tareq S Harb
    Cardiology Unit of the Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA
    Am J Cardiol 89:216-21. 2002
  22. ncbi request reprint Sympatholysis and cardiac sympathetic nerve function in the treatment of congestive heart failure
    Chang Seng Liang
    J Am Coll Cardiol 42:549-51. 2003

Research Grants4

  1. Norepinephrine and Nerve Growth Factor in Heart Failure
    Chang Seng Liang; Fiscal Year: 2004
    ..Our research will not only elucidate the mechanisms responsible for noradrenergic nerve ending dysfunction, but also provide a potentially useful new modality for the treatment of heart failure. ..