Fate tracing reveals the pericyte and not epithelial origin of myofibroblasts in kidney fibrosis.

By Benjamin D. Humphreys, Shuei-Liong Lin, Akio Kobayashi, Thomas Hudson, Brian T. Nowlin, Joseph V. Bonventre, M. T. Valerius, Andrew P. McMahon, Jeremy S. Duffield. American Journal of Pathology, 2010

1,446 citations recorded by the source corpus.

Subfields: Molecular Biology, Nephrology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/6126b0689d798fcf6997b01056d4493ddeaba6f3

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Citations in the corpus

Multiple stromal populations contribute to pulmonary fibrosis without evidence for epithelial to mesenchymal transition (2011, background): “Pericytes have recently been implicated as the origin of fibroblasts that secrete ECM in the context of renal fibrosis and scar tissue after spinal cord injury (18, 19, 33).”
Redefining the in vivo origin of metanephric nephron progenitors enables generation of complex kidney structures from pluripotent stem cells. (2014, background): “5 embryo contains another cell type, stromal cells, located in the outer layer of the nephron progenitors (Humphreys et al., 2010; Mugford et al., 2008b).”
Host Responses in Tissue Repair and Fibrosis (2012, background): “(22) adopted a genetic fate mapping approach.”
Cellular and molecular mechanisms in kidney fibrosis. (2014, neutral): “Studies of FOXD1-lineage cells have concluded that pericytes and resident fibroblasts are the major precursors of myofibroblasts, whereas others have concluded that equivalent cells in the kidney are resident fibroblasts (15, 22).”
Epithelial cell cycle arrest in G2/M mediates kidney fibrosis after injury (2010, positive): “, recent data indicate that fibrosis can occur in the absence of this cellular transformation proces”
Renal tubule injury: a driving force toward chronic kidney disease. (2018, background): “However, the contribution of EMT to kidney fibrosis remains a subject of debate, as studies using genetic cell lineage tracing could not find evidence of a direct contribution of epithelial cells to the myofibroblast population.(205) Two recent studies addressed this dispute and offered new insights”
Pathophysiology of Acute Kidney Injury (2012, neutral): “However, other investigators using similar approaches have not been able to confirm these data (218), so the role of EMT in interstitial fibrosis represents a controversial area.”
Perivascular Gli1+ progenitors are key contributors to injury-induced organ fibrosis (2014, neutral): “That myofibroblasts express PDGFRb+ has been known for many years (Asada et al., 2011; Humphreys et al., 2010; Kra- mann et al., 2013).”
Evolving challenges in hepatic fibrosis (2010, critical): “However, more recent studies refute this conclusion”
Recent developments in myofibroblast biology: paradigms for connective tissue remodeling. (2012, background): “Other interesting approaches are based on the possibility of terminating myofibroblast persistence by inducing their apoptosis(164) or their reversion to nonfibrogenic cell phenotypes.(108) In the case of the former, the ability of nitric oxide to induce myofibroblast apoptosis(165) suggests a possi”