W Kriz

Summary

Affiliation: University of Heidelberg
Country: Germany

Publications

  1. doi request reprint The podocyte's response to stress: the enigma of foot process effacement
    Wilhelm Kriz
    Centre for Biomedicine and Medical Technology Mannheim CBTM, Anatomy and Developmental Biology, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany
    Am J Physiol Renal Physiol 304:F333-47. 2013
  2. pmc Adenosine and ATP: traffic regulators in the kidney
    Wilhelm Kriz
    Department of Anatomy and Cell Biology, University of Heidelberg, Heidelberg, Germany
    J Clin Invest 114:611-3. 2004
  3. ncbi request reprint Pathways to nephron loss starting from glomerular diseases-insights from animal models
    Wilhelm Kriz
    Institute of Anatomy and Cell Biology, University of Heidelberg, Heidelberg, Germany
    Kidney Int 67:404-19. 2005
  4. ncbi request reprint Podocyte is the major culprit accounting for the progression of chronic renal disease
    Wilhelm Kriz
    Institut fur Anatomie und Zellbiologie, Universitat Heidelberg, D 69120 Heidelberg, Germany
    Microsc Res Tech 57:189-95. 2002
  5. ncbi request reprint TRPC6 - a new podocyte gene involved in focal segmental glomerulosclerosis
    Wilhelm Kriz
    Institut fur Anatomie und Zellbiologie, Universitat Heidelberg, INF 307, D69120 Heidelberg, Germany
    Trends Mol Med 11:527-30. 2005
  6. ncbi request reprint Tracer studies in the rat demonstrate misdirected filtration and peritubular filtrate spreading in nephrons with segmental glomerulosclerosis
    W Kriz
    Institut fur Anatomie und Zellbiologie, Universitat Heidelberg, Heidelberg, Germany
    J Am Soc Nephrol 12:496-506. 2001
  7. ncbi request reprint Ontogenetic development of the filtration barrier
    Wilhelm Kriz
    Anatomy and Cell Biology, Medical Faculty Mannheim, University of Heidelberg, Heidelberg, Germany
    Nephron Exp Nephrol 106:e44-50. 2007
  8. ncbi request reprint How does podocyte damage result in tubular damage?
    W Kriz
    Institut fur Anatomie und Zellbiologie, Universitat Heidelberg, Heidelberg, Germany
    Kidney Blood Press Res 22:26-36. 1999
  9. ncbi request reprint Pathways to recovery and loss of nephrons in anti-Thy-1 nephritis
    Wilhelm Kriz
    Institute of Anatomy and Cell Biology, University of Heidelberg, Im Neuenheimer Feld 307, D 69120 Heidelberg, Germany
    J Am Soc Nephrol 14:1904-26. 2003
  10. pmc Epithelial-mesenchymal transition (EMT) in kidney fibrosis: fact or fantasy?
    Wilhelm Kriz
    Department of Anatomy and Developmental Biology, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany
    J Clin Invest 121:468-74. 2011

Collaborators

Detail Information

Publications54

  1. doi request reprint The podocyte's response to stress: the enigma of foot process effacement
    Wilhelm Kriz
    Centre for Biomedicine and Medical Technology Mannheim CBTM, Anatomy and Developmental Biology, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany
    Am J Physiol Renal Physiol 304:F333-47. 2013
    ..We raise the hypothesis that foot process effacement represents a protective response of podocytes to escape detachment from the GBM...
  2. pmc Adenosine and ATP: traffic regulators in the kidney
    Wilhelm Kriz
    Department of Anatomy and Cell Biology, University of Heidelberg, Heidelberg, Germany
    J Clin Invest 114:611-3. 2004
    ..Facing the threat of urinary salt loss, this mechanism causes vasoconstriction and reduces filtration by generating adenosine through the hydrolysis of nucleotide precursors such as 5'-AMP and possibly ATP...
  3. ncbi request reprint Pathways to nephron loss starting from glomerular diseases-insights from animal models
    Wilhelm Kriz
    Institute of Anatomy and Cell Biology, University of Heidelberg, Heidelberg, Germany
    Kidney Int 67:404-19. 2005
    ..The only option for extracapillary injuries with tuft adhesion is repair by formation of a segmental adherent scar (i.e., segmental glomerulosclerosis)...
  4. ncbi request reprint Podocyte is the major culprit accounting for the progression of chronic renal disease
    Wilhelm Kriz
    Institut fur Anatomie und Zellbiologie, Universitat Heidelberg, D 69120 Heidelberg, Germany
    Microsc Res Tech 57:189-95. 2002
    ..It appears that the process that leads to the degeneration of a nephron in the context of "classic" FSGS always starts separately in the respective glomerulus by severe podocyte injury...
  5. ncbi request reprint TRPC6 - a new podocyte gene involved in focal segmental glomerulosclerosis
    Wilhelm Kriz
    Institut fur Anatomie und Zellbiologie, Universitat Heidelberg, INF 307, D69120 Heidelberg, Germany
    Trends Mol Med 11:527-30. 2005
    ....
  6. ncbi request reprint Tracer studies in the rat demonstrate misdirected filtration and peritubular filtrate spreading in nephrons with segmental glomerulosclerosis
    W Kriz
    Institut fur Anatomie und Zellbiologie, Universitat Heidelberg, Heidelberg, Germany
    J Am Soc Nephrol 12:496-506. 2001
    ....
  7. ncbi request reprint Ontogenetic development of the filtration barrier
    Wilhelm Kriz
    Anatomy and Cell Biology, Medical Faculty Mannheim, University of Heidelberg, Heidelberg, Germany
    Nephron Exp Nephrol 106:e44-50. 2007
    ..The last step in this development, the formation of the slit membrane, marks a caesura between diseases with early and late onset; all disorders without a properly developed slit membrane start prenatally or at birth...
  8. ncbi request reprint How does podocyte damage result in tubular damage?
    W Kriz
    Institut fur Anatomie und Zellbiologie, Universitat Heidelberg, Heidelberg, Germany
    Kidney Blood Press Res 22:26-36. 1999
    ..Therefore, histopathologically, 'classic' FSGS is best defined by an adhesion/synechia of the tuft to Bowman's capsule...
  9. ncbi request reprint Pathways to recovery and loss of nephrons in anti-Thy-1 nephritis
    Wilhelm Kriz
    Institute of Anatomy and Cell Biology, University of Heidelberg, Im Neuenheimer Feld 307, D 69120 Heidelberg, Germany
    J Am Soc Nephrol 14:1904-26. 2003
    ..No evidence emerged to suggest that the kind of focal interstitial proliferation associated with the degeneration of injured nephrons was harmful to a neighboring healthy nephron...
  10. pmc Epithelial-mesenchymal transition (EMT) in kidney fibrosis: fact or fantasy?
    Wilhelm Kriz
    Department of Anatomy and Developmental Biology, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany
    J Clin Invest 121:468-74. 2011
    ..Herein, we review and summarize both sides of this debate, but it is our view that unequivocal evidence supporting EMT as an in vivo process in kidney fibrosis is lacking...
  11. ncbi request reprint Rearrangements of the cytoskeleton and cell contacts induce process formation during differentiation of conditionally immortalized mouse podocyte cell lines
    P Mundel
    Department of Anatomy and Cell Biology, University of Heidelberg, Germany
    Exp Cell Res 236:248-58. 1997
    ..Therefore, the determinative steps of podocyte differentiation and process formation are studied for the first time using an inducible in vitro model...
  12. ncbi request reprint Podocyte injury underlies the progression of focal segmental glomerulosclerosis in the fa/fa Zucker rat
    N Gassler
    , , , Heidelberg, Germany
    Kidney Int 60:106-16. 2001
    ..Thus, each nephron entering this pathway to degeneration appears to start separately with the same initial injuries at the glomerulus...
  13. ncbi request reprint Induction of differentiation in cultured rat and human podocytes
    P Mundel
    Department of Anatomy and Cell Biology, University of Heidelberg, Germany
    J Am Soc Nephrol 8:697-705. 1997
    ..It was concluded that partial differentiation of cultured podocytes can be achieved simply by avoiding repeated subcultivation, resulting in an arborized phenotype more closely reflecting in vivo podocytes...
  14. pmc Effects of increased renal tubular vascular endothelial growth factor (VEGF) on fibrosis, cyst formation, and glomerular disease
    Samy Hakroush
    Centrum für Biomedizin und Medizintechnik Mannheim, University of Heidelberg, Germany
    Am J Pathol 175:1883-95. 2009
    ..Systemic VEGF lacks this effect, leading to severe deterioration in glomerular architecture, similar to that seen in diabetic nephropathy...
  15. ncbi request reprint Expression and signaling of parathyroid hormone-related protein in cultured podocytes
    N Endlich
    Institute of Anatomy and Cell Biology, University of Heidelberg, Germany
    Exp Nephrol 9:436-43. 2001
    ..However, PTHrP(1-36) attenuated the bradykinin-induced increase in [Ca2+]i. Our results suggest that PTHrP is an autocrine hormone in podocytes, which selectively activates the cAMP pathway through the PTH/PTHrP receptor...
  16. ncbi request reprint Progression of glomerular diseases: is the podocyte the culprit?
    W Kriz
    Institut fur Anatomie und Zellbiologie, Universitat Heidelberg, Germany
    Kidney Int 54:687-97. 1998
    ..The relevance of such filtration is as yet unclear but may play a considerable role in progression to global sclerosis and interstitial fibrosis...
  17. ncbi request reprint Update in podocyte biology
    K Endlich
    Institute for Anatomy and Cell Biology, University of Heidelberg, Heidelberg, Germany
    Curr Opin Nephrol Hypertens 10:331-40. 2001
    ..Efforts to understand molecular mechanisms causing these derangements are increasingly successful and will allow a better targeting of interventions to halt the progression of chronic renal disease...
  18. pmc Synaptopodin: an actin-associated protein in telencephalic dendrites and renal podocytes
    P Mundel
    Department of Anatomy and Cell Biology, University of Heidelberg, Germany
    J Cell Biol 139:193-204. 1997
    ....
  19. ncbi request reprint Podocytes populate cellular crescents in a murine model of inflammatory glomerulonephritis
    Marcus J Moeller
    Division of Nephrology, Department of Internal Medicine, University of Michigan, and Department of Veterans Affairs, Ann Arbor, Michigan, USA
    J Am Soc Nephrol 15:61-7. 2004
    ..Podocyte-specific antigens, including WT-1, synaptopodin, nephrin, and podocin, were not expressed by any cells in glomerular crescents, suggesting that podocytes underwent profound phenotypic changes in this nephritis model...
  20. ncbi request reprint Angiotensin II type 1 receptor overexpression in podocytes induces glomerulosclerosis in transgenic rats
    Sigrid Hoffmann
    Medical Research Center, Faculty for Clinical Medicine Mannheim, University of Heidelberg, Theodor Kutzer Ufer 1 3, Haus 8, Ebene 4, Mannheim 68135, Germany
    J Am Soc Nephrol 15:1475-87. 2004
    ..76) and urinary albumin excretion (r(2) = 0.70). The data provide direct evidence that increased AT1 signaling in podocytes leads to protein leakage and structural podocyte damage progressing to focal segmental glomerulosclerosis...
  21. ncbi request reprint An efficient system for tissue-specific overexpression of transgenes in podocytes in vivo
    Marcus J Moeller
    Institute for Anatomy and Cell Biology, University of Heidelberg, Germany
    Am J Physiol Renal Physiol 289:F481-8. 2005
    ..This approach should also circumvent common limitations arising from lethality or transgene silencing as a consequence of transgene overexpression...
  22. ncbi request reprint The pathogenesis of 'classic' focal segmental glomerulosclerosis-lessons from rat models
    Wilhelm Kriz
    lnstitut für Anatomie and Zellbiologle, Universitat Heidelberg, Heidelberg, Germany
    Nephrol Dial Transplant 18:vi39-44. 2003
    ..There is no nephron-to-nephron transfer of the disease at the level of the tubular interstitium...
  23. pmc Nonuniform microtubular polarity established by CHO1/MKLP1 motor protein is necessary for process formation of podocytes
    N Kobayashi
    Department of Anatomy and Cell Biology, University of Heidelberg, D 69120 Heidelberg, Germany
    J Cell Biol 143:1961-70. 1998
    ..Taken together, these findings lead to the conclusion that the nonuniform MT polarity in podocytes established by CHO1/MKLP1 is necessary for process formation...
  24. ncbi request reprint Structure and function of podocytes: an update
    P Mundel
    Department of Anatomy and Cell Biology I, University of Heidelberg, Germany
    Anat Embryol (Berl) 192:385-97. 1995
    ..A survey of podocyte function forms the center of this review. Finally, selected aspects of podocyte development and cell division are discussed...
  25. ncbi request reprint Cell biological and biochemical characterization of drebrin complexes in mesangial cells and podocytes of renal glomeruli
    Wiebke K Peitsch
    Division of Cell Biology, German Cancer Research Center, Heidelberg, Germany
    J Am Soc Nephrol 14:1452-63. 2003
    ..Clearly, drebrin has to be added to the ensemble of ABP regulating the actomyosin system and the dynamics of mesangial cells and foot processes in podocytes...
  26. ncbi request reprint CD2AP and p130Cas localize to different F-actin structures in podocytes
    T Welsch
    Institute of Anatomy and Cell Biology I, University of Heidelberg, INF 307, D-69120 Heidelberg, Germany
    Am J Physiol Renal Physiol 281:F769-77. 2001
    ..Whereas p130Cas is found in focal adhesions, CD2AP seems to be involved in the regulation of highly dynamic F-actin structures in podocyte foot processes...
  27. ncbi request reprint Stable expression of nephrin and localization to cell-cell contacts in novel murine podocyte cell lines
    Daniel Schiwek
    Department of Anatomy and Cell Biology, University of Heidelberg, Heidelberg, Germany
    Kidney Int 66:91-101. 2004
    ..To date, however, podocyte cell lines with stable expression of the crucial slit diaphragm protein nephrin and localization of nephrin to cell-cell contacts are not available...
  28. ncbi request reprint SCG/Kinjoh mice: a model of ANCA-associated crescentic glomerulonephritis with immune deposits
    Irmgard Neumann
    Fifth Department of Medicine, University Hospital Mannheim, Mannheim, Germany
    Kidney Int 64:140-8. 2003
    ..Since no systematic serologic, immunohistologic, or structural evaluation had been performed thus far, we reinvestigated the development of ANCA and CGN in these mice...
  29. pmc The LIM-homeodomain transcription factor Lmx1b plays a crucial role in podocytes
    Claudia Rohr
    Institute for Anatomy and Cell Biology I, University of Heidelberg, Im Neuenheimer Feld 307, 69120 Heidelberg, Germany
    J Clin Invest 109:1073-82. 2002
    ....
  30. ncbi request reprint Oligonephronia, not exuberant apoptosis, accounts for the development of glomerulosclerosis in the bcl-2 knockout mouse
    N Gassler
    Institut für Anatomie und Zellbiologie I, Universitat Heidelberg, Germany
    Nephrol Dial Transplant 13:2509-18. 1998
    ..The aim of the present study was to clarify whether the degenerative process in the kidneys seen after birth is based either on increased apoptosis of glomerular cells or on mechanisms independent from the genetic defect...
  31. ncbi request reprint Ganglioside GM2-activator protein and vesicular transport in collecting duct intercalated cells
    T M Mundel
    Department of Anatomy and Cell Biology, University of Heidelberg, Germany
    J Am Soc Nephrol 10:435-43. 1999
    ..In this study, a novel role for GM2-activator protein in intercalated cells is proposed, and possible roles in the shuttling mechanism are discussed...
  32. ncbi request reprint The role of the podocyte in glomerulosclerosis
    W Kriz
    Institut fur Anatomie und Zellbiologie, INF 307, Universitat Heidelberg, Germany
    Curr Opin Nephrol Hypertens 8:489-97. 1999
    ..The recently described 'collapsing' variant, in contrast, has an apparent excess of extracapillary cells, which may represent dedifferentiated, 'dysregulated' podocytes...
  33. ncbi request reprint Association of CD2AP with dynamic actin on vesicles in podocytes
    Thilo Welsch
    Department of Anatomy and Cell Biology, University of Heidelberg, D 69120 Heidelberg, Germany
    Am J Physiol Renal Physiol 289:F1134-43. 2005
    ....
  34. ncbi request reprint L-carnosine, a substrate of carnosinase-1, influences glucose metabolism
    Sibylle Sauerhöfer
    Institute for Anatomy and Cell Biology 1, University of Heidelberg, Heidelberg, Germany
    Diabetes 56:2425-32. 2007
    ..We therefore hypothesized that L-carnosine in the serum represents a critical protective factor in diabetic patients...
  35. ncbi request reprint Altered expression pattern of polycystin-2 in acute and chronic renal tubular diseases
    Nicholas Obermüller
    Medical Research Center, Klinikum Mannheim, University of Heidelberg, Mannheim, Germany
    J Am Soc Nephrol 13:1855-64. 2002
    ..After ischemia, polycystin-2 may be upregulated by the injured cells to protect themselves. It is unlikely that polycystin-2 plays a role in cyst formation in the (cy/+) rat and in the (pcy/pcy) mouse...
  36. ncbi request reprint Analysis of differential gene expression in stretched podocytes: osteopontin enhances adaptation of podocytes to mechanical stress
    Nicole Endlich
    Department of Anatomy and Cell Biology, University of Heidelberg, D 69120 Heidelberg, Germany
    FASEB J 16:1850-2. 2002
    ..This study delineates the molecular response of podocytes to mechanical stress and identifies OPN as a stretch-adapting molecule in podocytes...
  37. ncbi request reprint Podocytes are sensitive to fluid shear stress in vitro
    Colin Friedrich
    Department of Anatomy and Cell Biology I, University of Heidelberg, Heidelberg, Germany
    Am J Physiol Renal Physiol 291:F856-65. 2006
    ..Our data demonstrate that podocytes are highly sensitive to fluid shear stress. Shear stress induces a reorganization of the actin cytoskeleton and activates specific tyrosine kinases that are required to withstand fluid shear stress...
  38. ncbi request reprint Movement of stress fibers away from focal adhesions identifies focal adhesions as sites of stress fiber assembly in stationary cells
    Nicole Endlich
    Department of Anatomy and Cell Biology, Ernst Moritz Arndt University, D 17487 Greifswald, Germany
    Cell Motil Cytoskeleton 64:966-76. 2007
    ..Our finding of SF assembly at FAs has important implications for SF formation, force transmission, and tension distribution within the actin cytoskeletal network of stationary cells...
  39. doi request reprint Palladin is a dynamic actin-associated protein in podocytes
    Nicole Endlich
    Department of Anatomy and Cell Biology, University of Greifswald, Greifswald, Germany
    Kidney Int 75:214-26. 2009
    ..Our study shows that palladin is expressed in podocytes and plays an important role in actin dynamics...
  40. ncbi request reprint Differentially spliced isoforms of FAT1 are asymmetrically distributed within migrating cells
    Gerald S Braun
    Institute for Anatomy and Cell Biology 1, University of Heidelberg, 69120 Heidelberg, Germany
    J Biol Chem 282:22823-33. 2007
    ..In summary, FAT1(WT) is the only FAT1 isoform located along the cellular leading edge. Only FAT1(WT) is up-regulated in migration, induces cellular process formation when overexpressed, and is necessary for efficient wound healing...
  41. ncbi request reprint Progression of chronic renal failure in focal segmental glomerulosclerosis: consequence of podocyte damage or of tubulointerstitial fibrosis?
    Wilhelm Kriz
    Pediatr Nephrol 18:617-22. 2003
    ..The deleterious effects of protein leakage on progression appear to be a result of podocyte damage, the beneficial effects of ACE inhibitors a result of podocyte protection...
  42. pmc An efficient and versatile system for acute and chronic modulation of renal tubular function in transgenic mice
    Milena Traykova-Brauch
    Department of Cellular and Molecular Pathology, Deutsches Krebsforschungszentrum, Im Neuenheimer Feld 280, 69120 Heidelberg, Germany
    Nat Med 14:979-84. 2008
    ..These experiments establish Pax8-rtTA mice as a powerful tool for modeling renal diseases in transgenic mice...
  43. ncbi request reprint Abrogation of protein uptake through megalin-deficient proximal tubules does not safeguard against tubulointerstitial injury
    Franziska Theilig
    Institut für Vegetative Anatomie, Charite Universitatsmedizin Berlin, Philippstrasse 12, 10115 Berlin
    J Am Soc Nephrol 18:1824-34. 2007
    ....
  44. ncbi request reprint New insights into structural patterns encountered in glomerulosclerosis
    Michel LeHir
    Anatomical Institute, University of Zurich, Zurich, Switzerland
    Curr Opin Nephrol Hypertens 16:184-91. 2007
    ..Our aim was to survey those models in an attempt to discover correlations between histopathological patterns and pathogenic mechanisms...
  45. ncbi request reprint In mice, proteinuria and renal inflammatory responses to albumin overload are strain-dependent
    David A Ishola
    Department of Nephrology, University Medical Center, Utrecht, The Netherlands
    Nephrol Dial Transplant 21:591-7. 2006
    ..Albumin overload, an important model of proteinuric disease, induces marked proteinuria in rats but barely in C57BL/6 mice. We hypothesized that albumin overload would induce more proteinuria in 129S2/Sv than C57BL/6J mice...
  46. ncbi request reprint Podocytes as a target for treatment with ACE inhibitors and/or angiotensin-receptor blockers
    Wilhelm Kriz
    Kidney Int 65:333-4. 2004
  47. ncbi request reprint The Tie-2 ligand angiopoietin-2 is stored in and rapidly released upon stimulation from endothelial cell Weibel-Palade bodies
    Ulrike Fiedler
    Department of Vascular Biology and Angiogenesis Research Tumor Biology Center, Breisacher Str 117, 79106 Freiburg, Germany
    Blood 103:4150-6. 2004
    ....
  48. ncbi request reprint Cell biology of the glomerular podocyte
    Hermann Pavenstadt
    Division of Nephrology, Department of Medicine, University Hospital Freiburg, Freiburg, Germany
    Physiol Rev 83:253-307. 2003
    ..This review integrates our recent physiological and molecular understanding of the role of podocytes during the maintenance and failure of the glomerular filtration barrier...
  49. ncbi request reprint C-type natriuretic peptide as a podocyte hormone and modulation of its cGMP production by glucose and mechanical stress
    Barbara Lewko
    Department of Immunopathology, Medical University of Gdansk, Gdansk, Poland
    Kidney Int 66:1001-8. 2004
    ..We investigated whether mechanical stress and high ambient glucose influence cGMP generation in podocytes stimulated with NPs. Additionally, the C-type natriuretic peptide (CNP) system has been characterized in these cells...
  50. doi request reprint Fenestrated glomerular capillaries are unique
    Wilhelm Kriz
    J Am Soc Nephrol 19:1439-40. 2008
  51. ncbi request reprint Characterization of glucose uptake by cultured rat podocytes
    Barbara Lewko
    Department of Immunopathology, Medical University of Gdansk, Gdansk, Poland
    Kidney Blood Press Res 28:1-7. 2005
    ..It seems likely that a sodium-dependent glucose cotransporter may also be present in these cells...
  52. ncbi request reprint Hypertrophy of podocytes: a mechanism to cope with increased glomerular capillary pressures?
    Wilhelm Kriz
    Kidney Int 67:373-4. 2005
  53. ncbi request reprint Introduction to the podocyte issue: more than eight enigmas
    Naoto Kobayashi
    Department of Anatomy and Embryology, Ehime University School of Medicine, Ehime, 791 0295 Japan
    Microsc Res Tech 57:187-8. 2002
  54. ncbi request reprint Lack of connexin 40 causes displacement of renin-producing cells from afferent arterioles to the extraglomerular mesangium
    Lisa Kurtz
    Physiologisches Institut der Universität Regensburg, D 93040 Regensburg, Germany
    J Am Soc Nephrol 18:1103-11. 2007
    ..Moreover, these findings support the notion that gap junctions are relevant for the macula densa signaling to renin-producing cells...