Sources of myofibroblasts in kidney fibrosis
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Sources of myofibroblasts in kidney fibrosis : all answers are correct, however to different extent! / Ballhause, Tobias M; Soldati, Rocío; Mertens, Peter R.
In: INT UROL NEPHROL, Vol. 46, No. 3, 03.2014, p. 659-64.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Sources of myofibroblasts in kidney fibrosis
T2 - all answers are correct, however to different extent!
AU - Ballhause, Tobias M
AU - Soldati, Rocío
AU - Mertens, Peter R
PY - 2014/3
Y1 - 2014/3
N2 - Most inflammatory kidney diseases have the final outcome of fibrosis with the loss of kidney architecture and progressive loss of kidney function. Excess matrix deposition is observed, which may be an inadequate attempt to limit organ damage. The primary sources of matrix synthesis are resident cells that may acquire different activated phenotypes and likely orchestrate matrix deposition. Over the last decades, intense efforts were undertaken to define the origin of myofibroblasts, resulting in four different controversially discussed hypotheses: bone marrow recruitment, vascular pericyte-derived myofibroblasts, epithelial-to-mesenchymal transition (EMT), and endothelial-to-mesenchymal transition (EndMT). In a recent article, LeBleu et al. (Nat Med 19(8):1047-1053, 2013) address this issue and come to the conclusion that most of the different hypotheses are likely true, however to different extents. To arrive at this conclusion, the authors have performed genetic cell tracking and quantification by cell labeling in newly generated knockout mouse models. Quantitative analyses have been made and yield the following estimates: 50% of the myofibroblasts are derived through proliferation from resident fibroblasts, 35% differentiate from bone marrow-derived cells, 10% arise from EndMT, and 5% through EMT.
AB - Most inflammatory kidney diseases have the final outcome of fibrosis with the loss of kidney architecture and progressive loss of kidney function. Excess matrix deposition is observed, which may be an inadequate attempt to limit organ damage. The primary sources of matrix synthesis are resident cells that may acquire different activated phenotypes and likely orchestrate matrix deposition. Over the last decades, intense efforts were undertaken to define the origin of myofibroblasts, resulting in four different controversially discussed hypotheses: bone marrow recruitment, vascular pericyte-derived myofibroblasts, epithelial-to-mesenchymal transition (EMT), and endothelial-to-mesenchymal transition (EndMT). In a recent article, LeBleu et al. (Nat Med 19(8):1047-1053, 2013) address this issue and come to the conclusion that most of the different hypotheses are likely true, however to different extents. To arrive at this conclusion, the authors have performed genetic cell tracking and quantification by cell labeling in newly generated knockout mouse models. Quantitative analyses have been made and yield the following estimates: 50% of the myofibroblasts are derived through proliferation from resident fibroblasts, 35% differentiate from bone marrow-derived cells, 10% arise from EndMT, and 5% through EMT.
KW - Animals
KW - Fibrosis
KW - Humans
KW - Kidney/pathology
KW - Myofibroblasts/cytology
U2 - 10.1007/s11255-013-0626-5
DO - 10.1007/s11255-013-0626-5
M3 - SCORING: Journal article
C2 - 24368748
VL - 46
SP - 659
EP - 664
JO - INT UROL NEPHROL
JF - INT UROL NEPHROL
SN - 0301-1623
IS - 3
ER -