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Frontiers in Nephrology
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Renal Fibroblasts and Myofibroblasts in Chronic Kidney Disease

Frank Strutz and Michael Zeisberg
JASN November 2006, 17 (11) 2992-2998; DOI: https://doi.org/10.1681/ASN.2006050420
Frank Strutz
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Michael Zeisberg
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    Figure 1.

    Activation of resident fibroblasts by stimuli associated with tissue injury.

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    Figure 2.

    Possible origin of matrix-producing cells in the kidney.

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    Table 1.

    Cell types with mesenchymal phenotypes detected in the kidneya

    Cell TypeMarkersSpecific CharacteristicsReferences
    Resident FibroblastsFSP1, HSP47, 5′ectonucleotidase, CD44, ICAM, DDR2Phenotypic variability between cortical and medullary fibroblasts41, 44, 63
    Myofibroblastsα-SMA13
    Pericytesα-SMA, NG2, PDGFR-2, DesminAssociated capillaries and venoles64, 65
    Vascular smooth muscle cellsα-SMA, caldesmon, calponinAssociated arteries, arterioles, veins64
    EMT-derived fibroblastsFSP1 (residual epithelial markers?)Exclusively found in fibrotic kidneys41, 44
    Mesenchymal stem cellsFSP1?44
    • ↵a At least 6 distinct cell types with mesenchymal phenotypes can be detected in the kidney. Due to the lack of specific markers, identification of the different lineages can be challenging. In the normal kidney, myofibroblasts can be distinguished from vascular smooth muscle cells and pericytes based on topographical criteria. Without genetic markers, indisputable identification of EMT-derived cells and mesenchymal stem cells is not feasible as of yet. HSP47, heat shock protein 47; ICAM, intracellular adhesion molecule; DDR2, discoidin domain receptor; α-SMA, α-smooth muscle actin; NG2, neuron glial antigen 2; PDGFR, PDGF receptor; EMT, epithelial–mesenchymal transition.

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Journal of the American Society of Nephrology: 17 (11)
Journal of the American Society of Nephrology
Vol. 17, Issue 11
November 2006
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Renal Fibroblasts and Myofibroblasts in Chronic Kidney Disease
Frank Strutz, Michael Zeisberg
JASN Nov 2006, 17 (11) 2992-2998; DOI: 10.1681/ASN.2006050420

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Renal Fibroblasts and Myofibroblasts in Chronic Kidney Disease
Frank Strutz, Michael Zeisberg
JASN Nov 2006, 17 (11) 2992-2998; DOI: 10.1681/ASN.2006050420
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  • Polycystic Kidney Disease
  • Genotype–Phenotype Correlations in Autosomal Dominant and Autosomal Recessive Polycystic Kidney Disease
  • Role of Primary Cilia in the Pathogenesis of Polycystic Kidney Disease
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  • TLR4 Promotes Fibrosis but Attenuates Tubular Damage in Progressive Renal Injury
  • Identification of Epithelial to Mesenchymal Transition as a Novel Source of Fibroblasts in Intestinal Fibrosis
  • Inhibition of Integrin-Linked Kinase Attenuates Renal Interstitial Fibrosis
  • Renal fibrosis is attenuated by targeted disruption of KCa3.1 potassium channels
  • Fibroblasts in Kidney Fibrosis Emerge via Endothelial-to-Mesenchymal Transition
  • tPA Protects Renal Interstitial Fibroblasts and Myofibroblasts from Apoptosis
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