Anje Cauwels

Summary

Affiliation: Ghent University
Country: Belgium

Publications

  1. ncbi Nitric oxide in shock
    A Cauwels
    Department for Molecular Biomedical Research, VIB, Technologiepark 927, B 9052 Ghent, Belgium
    Kidney Int 72:557-65. 2007
  2. doi Nitric oxide production by endotoxin preparations in TLR4-deficient mice
    Anje Cauwels
    Department for Molecular Biomedical Research, VIB, B 9052 Ghent, Belgium Department of Biomedical Molecular Biology, Ghent University, B 9052 Ghent, Belgium Electronic address
    Nitric Oxide 36:36-43. 2014
  3. pmc Nitrite protects against morbidity and mortality associated with TNF- or LPS-induced shock in a soluble guanylate cyclase-dependent manner
    Anje Cauwels
    Department for Molecular Biomedical Research, Flanders Institute for Biotechnology, 9052 Ghent, Belgium
    J Exp Med 206:2915-24. 2009
  4. ncbi Dual role of endogenous nitric oxide in tumor necrosis factor shock: induced NO tempers oxidative stress
    A Cauwels
    Molecular Pathophysiology and Experimental Therapy Unit, Department for Molecular Biomedical Research, Ghent University and Flanders Interuniversity Institute for Biotechnology VIB, Ghent, Zwijnaarde, Belgium
    Cell Mol Life Sci 62:1632-40. 2005
  5. pmc Anaphylactic shock depends on PI3K and eNOS-derived NO
    Anje Cauwels
    Molecular Pathophysiology and Experimental Therapy Unit, Department for Molecular Biomedical Research, Ghent University, Belgium, and Cardiovascular Research Center, Massachusetts General Hospital, Charlestown, USA
    J Clin Invest 116:2244-51. 2006
  6. ncbi Critical role for small and large conductance calcium-dependent potassium channels in endotoxemia and TNF toxicity
    Anje Cauwels
    Department for Molecular Biomedical Research, Ghent University, Ghent, Belgium
    Shock 29:577-82. 2008
  7. ncbi Survival of TNF toxicity: dependence on caspases and NO
    Anje Cauwels
    Department for Molecular Biomedical Research, VIB, B 9052 Ghent, Belgium
    Arch Biochem Biophys 462:132-9. 2007
  8. pmc sGC(alpha)1(beta)1 attenuates cardiac dysfunction and mortality in murine inflammatory shock models
    Emmanuel S Buys
    Department of Anesthesia and Critical Care, Cardiology Division, Anesthesia Center for Critical Care Research, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA
    Am J Physiol Heart Circ Physiol 297:H654-63. 2009
  9. ncbi Caspase inhibition causes hyperacute tumor necrosis factor-induced shock via oxidative stress and phospholipase A2
    Anje Cauwels
    Molecular Pathophysiology and Experimental Therapy Unit, Department for Molecular Biomedical Research, Ghent University and Flanders Interuniversity Institute for Biotechnology, Ghent, Belgium
    Nat Immunol 4:387-93. 2003
  10. pmc The soluble guanylate cyclase activator BAY 58-2667 protects against morbidity and mortality in endotoxic shock by recoupling organ systems
    Benjamin Vandendriessche
    Department for Molecular Biomedical Research, VIB, Ghent, Belgium Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium
    PLoS ONE 8:e72155. 2013

Collaborators

Detail Information

Publications20

  1. ncbi Nitric oxide in shock
    A Cauwels
    Department for Molecular Biomedical Research, VIB, Technologiepark 927, B 9052 Ghent, Belgium
    Kidney Int 72:557-65. 2007
    ..Amongst these, high hopes are set for selective iNOS inhibitors. But it might also be necessary to shift gears and focus on downstream cardiovascular targets of NO or on other vasodilating phenomena...
  2. doi Nitric oxide production by endotoxin preparations in TLR4-deficient mice
    Anje Cauwels
    Department for Molecular Biomedical Research, VIB, B 9052 Ghent, Belgium Department of Biomedical Molecular Biology, Ghent University, B 9052 Ghent, Belgium Electronic address
    Nitric Oxide 36:36-43. 2014
    ..Surprisingly, the excessive iNOS-derived systemic NO production induced by impure LPS in TLR4⁻/⁻ is not accompanied by hypotension or morbidity...
  3. pmc Nitrite protects against morbidity and mortality associated with TNF- or LPS-induced shock in a soluble guanylate cyclase-dependent manner
    Anje Cauwels
    Department for Molecular Biomedical Research, Flanders Institute for Biotechnology, 9052 Ghent, Belgium
    J Exp Med 206:2915-24. 2009
    ..In conclusion, we show that nitrite can protect against toxicity in shock via sGC-dependent signaling, which may include hypoxic vasodilation necessary to maintain microcirculation and organ function, and cardioprotection...
  4. ncbi Dual role of endogenous nitric oxide in tumor necrosis factor shock: induced NO tempers oxidative stress
    A Cauwels
    Molecular Pathophysiology and Experimental Therapy Unit, Department for Molecular Biomedical Research, Ghent University and Flanders Interuniversity Institute for Biotechnology VIB, Ghent, Zwijnaarde, Belgium
    Cell Mol Life Sci 62:1632-40. 2005
    ..Together, these in vivo results indicate that induced NO not only causes hemodynamic collapse, but is also essential for curbing TNF-induced oxidative stress, which appears to hinge on PLA2-dependent mechanisms...
  5. pmc Anaphylactic shock depends on PI3K and eNOS-derived NO
    Anje Cauwels
    Molecular Pathophysiology and Experimental Therapy Unit, Department for Molecular Biomedical Research, Ghent University, Belgium, and Cardiovascular Research Center, Massachusetts General Hospital, Charlestown, USA
    J Clin Invest 116:2244-51. 2006
    ....
  6. ncbi Critical role for small and large conductance calcium-dependent potassium channels in endotoxemia and TNF toxicity
    Anje Cauwels
    Department for Molecular Biomedical Research, Ghent University, Ghent, Belgium
    Shock 29:577-82. 2008
    ..Our results point to SK and BK channels as potential targets in septic shock treatment to be modulated preferentially together with sGC...
  7. ncbi Survival of TNF toxicity: dependence on caspases and NO
    Anje Cauwels
    Department for Molecular Biomedical Research, VIB, B 9052 Ghent, Belgium
    Arch Biochem Biophys 462:132-9. 2007
    ..In addition, our results also indicate that caspases may exert an important endogenous negative feedback on oxidative stress as well...
  8. pmc sGC(alpha)1(beta)1 attenuates cardiac dysfunction and mortality in murine inflammatory shock models
    Emmanuel S Buys
    Department of Anesthesia and Critical Care, Cardiology Division, Anesthesia Center for Critical Care Research, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA
    Am J Physiol Heart Circ Physiol 297:H654-63. 2009
    ..Together, these findings suggest that cGMP generated by sGC(alpha)(1)beta(1) protects against cardiac dysfunction and mortality in murine inflammatory shock models...
  9. ncbi Caspase inhibition causes hyperacute tumor necrosis factor-induced shock via oxidative stress and phospholipase A2
    Anje Cauwels
    Molecular Pathophysiology and Experimental Therapy Unit, Department for Molecular Biomedical Research, Ghent University and Flanders Interuniversity Institute for Biotechnology, Ghent, Belgium
    Nat Immunol 4:387-93. 2003
    ..In addition, survival of TNF toxicity seemed to require a caspase-dependent protective feedback on excessive reactive oxygen species (ROS) formation and phospholipase A2 activation...
  10. pmc The soluble guanylate cyclase activator BAY 58-2667 protects against morbidity and mortality in endotoxic shock by recoupling organ systems
    Benjamin Vandendriessche
    Department for Molecular Biomedical Research, VIB, Ghent, Belgium Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium
    PLoS ONE 8:e72155. 2013
    ..We speculate that, considering the central role of sGC signaling in many pathways required for maintenance of (micro)circulatory homeostasis, BAY 58-2667 supports organ function by recoupling inter-organ communication pathways. ..
  11. ncbi TLR2 activation causes no morbidity or cardiovascular failure, despite excessive systemic nitric oxide production
    Anje Cauwels
    Department for Molecular Biomedical Research, VIB, Technologiepark 927, Ghent B 9052, Belgium
    Cardiovasc Res 100:28-35. 2013
    ..In addition, NOS produce superoxide in case of substrate or cofactor deficiency or oxidation. We hypothesized that excessive systemic iNOS-derived NO production is insufficient to trigger cardiovascular failure and shock...
  12. ncbi The in vivo contribution of hematopoietic cells to systemic TNF and IL-6 production during endotoxemia
    Jennyfer Bultinck
    Molecular Pathophysiology and Experimental Therapy Unit, Department of Molecular Biomedical Research, Ghent University and Flanders Interuniversity Institute of Biotechnology VIB, Ghent Zwijnaarde, Belgium
    Cytokine 36:160-6. 2006
    ..Moreover, LPS-induced IL-6 production in parenchymal cells may be partially mediated by the TNF/TNF-R1 pathway as evidenced by the systemic IL-6 levels in LPS-treated wild type (WT), TNF-R1-deficient and chimeric mice...
  13. ncbi Systemic NO production during (septic) shock depends on parenchymal and not on hematopoietic cells: in vivo iNOS expression pattern in (septic) shock
    Jennyfer Bultinck
    Department for Molecular Biomedical Research, Ghent University VIB, Technologiepark 927, Ghent 9052, Belgium
    FASEB J 20:2363-5. 2006
    ....
  14. pmc Reactive oxygen species and small-conductance calcium-dependent potassium channels are key mediators of inflammation-induced hypotension and shock
    Anje Cauwels
    Department for Molecular Biomedical Research, VIB, Technologiepark 927, 9052 Ghent, Belgium
    J Mol Med (Berl) 88:921-30. 2010
    ..Moreover, they may also explain why antioxidants other than tempol fail to provide survival benefit during shock...
  15. doi Simultaneous targeting of IL-1 and IL-18 is required for protection against inflammatory and septic shock
    Tom Vanden Berghe
    1 Inflammation Research Center, VIB, Ghent, Belgium
    Am J Respir Crit Care Med 189:282-91. 2014
    ..Conclusions: Our data point toward the therapeutic potential of neutralizing IL-1 and IL-18 simultaneously in sepsis, rather than inhibiting the upstream inflammatory caspases. ..
  16. doi Nitrite regulation of shock
    Anje Cauwels
    Department for Molecular Biomedical Research, VIB, Technologiepark 927, B 9052, Ghent, Belgium
    Cardiovasc Res 89:553-9. 2011
    ....
  17. doi Severity of sepsis-induced acute kidney injury in a novel mouse model is age dependent
    Bert Maddens
    Department of Pharmacology, Toxicology and Biochemistry, Ghent University, Ghent, Belgium
    Crit Care Med 40:2638-46. 2012
    ..In addition, the age dependency of the severity of sepsis and sepsis-induced AKI was studied by validating this model in three different age categories...
  18. ncbi Protection against TNF-induced lethal shock by soluble guanylate cyclase inhibition requires functional inducible nitric oxide synthase
    A Cauwels
    MPET, Department of Molecular Biology, Flanders Interuniversity Institute for Biotechnology, Ghent University, Belgium
    Immunity 13:223-31. 2000
    ..These data imply that iNOS- (and not eNOS-) derived NO is an endogenous protective molecule indispensable to survive a TNF challenge and exerting this beneficial effect via sGC-independent mechanisms...
  19. doi RIP kinase-dependent necrosis drives lethal systemic inflammatory response syndrome
    Linde Duprez
    Department for Molecular Biomedical Research, the Flanders Institute for Biotechnology VIB, 9052 Ghent, Belgium
    Immunity 35:908-18. 2011
    ....
  20. pmc IL-17 produced by Paneth cells drives TNF-induced shock
    Nozomi Takahashi
    Rheumatology Research and Advanced Therapeutics, Radboud University Nijmegen Medical Centre, 6500 HB Nijmegen, Netherlands
    J Exp Med 205:1755-61. 2008
    ..These data indicate that innate immune cytokine responses in the local mucosa may participate in rapidly amplifying responses to systemic inflammatory challenges...