Wilfred Lieberthal

Summary

Affiliation: State University of New York
Country: USA

Publications

  1. doi request reprint The role of the mammalian target of rapamycin (mTOR) in renal disease
    Wilfred Lieberthal
    Stony Brook Medical Center, Health Sciences Center, 16 081B Nicholls Road, Stony Brook, NY 11794 8166, USA
    J Am Soc Nephrol 20:2493-502. 2009
  2. ncbi request reprint Rapamycin delays but does not prevent recovery from acute renal failure: role of acquired tubular resistance
    Wilfred Lieberthal
    Department of Nephrology, Health Science Center, Stony Brook University Hospital, Stony Brook, NY 11794 0001, USA
    Transplantation 82:17-22. 2006
  3. ncbi request reprint Macroautophagy: a mechanism for mediating cell death or for promoting cell survival?
    Wilfred Lieberthal
    Stony Brook University Hospital, Department of Medicine, Stony Brook, New York, USA
    Kidney Int 74:555-7. 2008
  4. pmc Recognition-dependent signaling events in response to apoptotic targets inhibit epithelial cell viability by multiple mechanisms: implications for non-immune tissue homeostasis
    Vimal A Patel
    Section of Nephrology, Department of Medicine, University of Illinois, Chicago, Illinois 60612, USA
    J Biol Chem 287:13761-77. 2012
  5. pmc Recognition of apoptotic cells by epithelial cells: conserved versus tissue-specific signaling responses
    Vimal A Patel
    Section of Nephrology, Department of Medicine, University of Illinois, Chicago, Illinois 60612, USA
    J Biol Chem 285:1829-40. 2010
  6. doi request reprint Mammalian target of rapamycin and the kidney. II. Pathophysiology and therapeutic implications
    Wilfred Lieberthal
    Stony Brook Univ Medical Center, Health Sciences Center, Stony Brook, NY 11794 8166, USA
    Am J Physiol Renal Physiol 303:F180-91. 2012
  7. pmc AMPK protects proximal tubular cells from stress-induced apoptosis by an ATP-independent mechanism: potential role of Akt activation
    Wilfred Lieberthal
    Dept of Medicine, Stony Brook Medical Center, 101 Nicholls Rd, Stony Brook, NY 11794 8166, USA
    Am J Physiol Renal Physiol 301:F1177-92. 2011
  8. pmc Susceptibility to ATP depletion of primary proximal tubular cell cultures derived from mice lacking either the α1 or the α2 isoform of the catalytic domain of AMPK
    Wilfred Lieberthal
    Department of Medicine, Stony Brook University Medical Center, Stony Brook, NY 11794, USA
    BMC Nephrol 14:251. 2013
  9. doi request reprint Mammalian target of rapamycin and the kidney. I. The signaling pathway
    Wilfred Lieberthal
    Department of Medicine, Stony Brook University Medical Center, Stony Brook, NY, USA
    Am J Physiol Renal Physiol 303:F1-10. 2012
  10. ncbi request reprint Role of apoptosis in the pathogenesis of acute renal failure
    Ramon Bonegio
    Renal Section, Department of Medicine, Boston Medical Center, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    Curr Opin Nephrol Hypertens 11:301-8. 2002

Collaborators

Detail Information

Publications20

  1. doi request reprint The role of the mammalian target of rapamycin (mTOR) in renal disease
    Wilfred Lieberthal
    Stony Brook Medical Center, Health Sciences Center, 16 081B Nicholls Road, Stony Brook, NY 11794 8166, USA
    J Am Soc Nephrol 20:2493-502. 2009
    ..Finally, inhibitors of mTOR improve survival in patients with metastatic renal cell carcinoma...
  2. ncbi request reprint Rapamycin delays but does not prevent recovery from acute renal failure: role of acquired tubular resistance
    Wilfred Lieberthal
    Department of Nephrology, Health Science Center, Stony Brook University Hospital, Stony Brook, NY 11794 0001, USA
    Transplantation 82:17-22. 2006
    ..We reported that rapamycin impairs recovery after acute renal failure (ARF) in rats. The objective of this study was to determine if recovery will eventually occur after ARF despite continued rapamycin treatment...
  3. ncbi request reprint Macroautophagy: a mechanism for mediating cell death or for promoting cell survival?
    Wilfred Lieberthal
    Stony Brook University Hospital, Department of Medicine, Stony Brook, New York, USA
    Kidney Int 74:555-7. 2008
    ..This finding provides novel evidence that autophagy may play a role in ameliorating the effects of acute injury on the kidney...
  4. pmc Recognition-dependent signaling events in response to apoptotic targets inhibit epithelial cell viability by multiple mechanisms: implications for non-immune tissue homeostasis
    Vimal A Patel
    Section of Nephrology, Department of Medicine, University of Illinois, Chicago, Illinois 60612, USA
    J Biol Chem 287:13761-77. 2012
    ..g. breast-derived) show increased viability. By acting as sentinels of environmental change, apoptotic targets allow neighboring cells, especially non-migratory epithelial cells, to monitor and potentially adapt to local stresses...
  5. pmc Recognition of apoptotic cells by epithelial cells: conserved versus tissue-specific signaling responses
    Vimal A Patel
    Section of Nephrology, Department of Medicine, University of Illinois, Chicago, Illinois 60612, USA
    J Biol Chem 285:1829-40. 2010
    ..By acting as sentinels of environmental change, apoptotic and necrotic targets may permit neighboring viable cells, especially non-migratory epithelial cells, to monitor and adapt to local stresses...
  6. doi request reprint Mammalian target of rapamycin and the kidney. II. Pathophysiology and therapeutic implications
    Wilfred Lieberthal
    Stony Brook Univ Medical Center, Health Sciences Center, Stony Brook, NY 11794 8166, USA
    Am J Physiol Renal Physiol 303:F180-91. 2012
    ....
  7. pmc AMPK protects proximal tubular cells from stress-induced apoptosis by an ATP-independent mechanism: potential role of Akt activation
    Wilfred Lieberthal
    Dept of Medicine, Stony Brook Medical Center, 101 Nicholls Rd, Stony Brook, NY 11794 8166, USA
    Am J Physiol Renal Physiol 301:F1177-92. 2011
    ..Protection by AMPK appears to be due not to AMPK-mediated conservation of cell energy stores, but rather, at least in part, to AMPK-mediated activation of Akt...
  8. pmc Susceptibility to ATP depletion of primary proximal tubular cell cultures derived from mice lacking either the α1 or the α2 isoform of the catalytic domain of AMPK
    Wilfred Lieberthal
    Department of Medicine, Stony Brook University Medical Center, Stony Brook, NY 11794, USA
    BMC Nephrol 14:251. 2013
    ..Previous studies, using an immortalized MPT cell line, suggest that AMPK is activated during metabolic stress, and ameliorates stress-induced apoptosis of these cells...
  9. doi request reprint Mammalian target of rapamycin and the kidney. I. The signaling pathway
    Wilfred Lieberthal
    Department of Medicine, Stony Brook University Medical Center, Stony Brook, NY, USA
    Am J Physiol Renal Physiol 303:F1-10. 2012
    ..Rapamycin and its analogs inhibit the activity of mTORC1 only, and not that of mTORC2, while the newer "catalytic" mTOR inhibitors affect both complexes...
  10. ncbi request reprint Role of apoptosis in the pathogenesis of acute renal failure
    Ramon Bonegio
    Renal Section, Department of Medicine, Boston Medical Center, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    Curr Opin Nephrol Hypertens 11:301-8. 2002
    ..In addition to caspase inhibition, the apoptotic pathway offers many potential targets for therapeutic interventions to prevent renal tubular cell apoptosis...
  11. pmc Apoptotic and necrotic cells as sentinels of local tissue stress and inflammation: response pathways initiated in nearby viable cells
    Vimal A Patel
    Section of Nephrology, Department of Medicine, The University of Illinois at Chicago, Chicago, IL 60612, USA
    Autoimmunity 42:317-21. 2009
    ..We propose that dead cells (apo and nec) act as sentinels to alert nearby viable cells to local environmental change or stress...
  12. ncbi request reprint Phagocytosis of apoptotic cells by macrophages induces novel signaling events leading to cytokine-independent survival and inhibition of proliferation: activation of Akt and inhibition of extracellular signal-regulated kinases 1 and 2
    Suman M Reddy
    Renal Section, Evans Memorial Department of Clinical Research, Department of Medicine, Boston University Medical Center, Boston, MA 02118, USA
    J Immunol 169:702-13. 2002
    ..These signaling differences may underlie the opposing tendencies of apoptotic cells and danger signals in promoting tolerance vs immunity...
  13. ncbi request reprint Chemical anoxia of tubular cells induces activation of c-Src and its translocation to the zonula adherens
    Diviya Sinha
    Renal Section, Evans Biomedical Research Center, Department of Medicine, Boston Medical Center and Boston University School of Medicine, Boston, Massachusetts 02118, USA
    Am J Physiol Renal Physiol 284:F488-97. 2003
    ..Our findings suggest that these events contribute to the loss of the epithelial barrier function associated with chemical anoxia...
  14. ncbi request reprint Acute renal failure in the critically ill patient
    Vivian E Abernethy
    Boston University School of Medicine, Renal Section, Evans Biomedical Research Center, 5th Floor, Room 537, 650 Albany Street, Boston, MA 02118, USA
    Crit Care Clin 18:203-22, v. 2002
    ..In addition, some unusual causes of acute renal failure that occur predominantly in the intensive care unit are briefly discussed...
  15. ncbi request reprint Risk factors for acute renal failure: inherent and modifiable risks
    Martine Leblanc
    Department of Nephrology, University of Montreal, Montreal, Canada
    Curr Opin Crit Care 11:533-6. 2005
    ..Our purpose is to discuss established risk factors in the development of acute renal failure and briefly overview clinical markers and preventive measures...
  16. ncbi request reprint Inhibition of ligand-independent ERK1/2 activity in kidney proximal tubular cells deprived of soluble survival factors up-regulates Akt and prevents apoptosis
    Diviya Sinha
    Renal Section, Boston Medical Center, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    J Biol Chem 279:10962-72. 2004
    ....
  17. ncbi request reprint Lithium activates the Wnt and phosphatidylinositol 3-kinase Akt signaling pathways to promote cell survival in the absence of soluble survival factors
    Diviya Sinha
    Renal Section, Evans Biomedical Research Center, Rm 546, 650 Albany St, Boston, MA 02118, USA
    Am J Physiol Renal Physiol 288:F703-13. 2005
    ..Extracellular IGF-II serves as an autocrine survival factor that is responsible, in part, for activating the anti-apoptotic phosphatidylinositol-3-kinase-Akt pathway during serum deprivation...
  18. ncbi request reprint Rapamycin ameliorates proteinuria-associated tubulointerstitial inflammation and fibrosis in experimental membranous nephropathy
    Ramon G B Bonegio
    Evans Biomedical Research Center, Room X530, Boston University Medical Center, 650 Albany Street, Boston, MA 02129, USA
    J Am Soc Nephrol 16:2063-72. 2005
    ..Rapamycin also completely inhibited compensatory renal hypertrophy. In summary, rapamycin ameliorates the tubulointerstitial disease associated with chronic proteinuria and loss of renal mass...
  19. ncbi request reprint Primary prevention of acute renal failure in the critically ill
    John A Kellum
    Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA
    Curr Opin Crit Care 11:537-41. 2005
    ..To date, no therapy apart from renal replacement therapy has been shown to improve survival or enhance recover. Thus, efforts to prevent acute renal failure are eagerly sought...
  20. ncbi request reprint Comparison of the effects of a 50% exchange-transfusion with albumin, hetastarch, and modified hemoglobin solutions
    Wilfred Lieberthal
    Evans Department of Clinical Research, Boston University Medical Center, Massachusetts, USA
    Shock 17:61-9. 2002
    ..We conclude, that of all solutions tested, both the short- and long-term effects of an exchange-transfusion with whole blood are most closely reproduced by an exchange with o-raffinose-crosslinked hemoglobin...