Blockade of PDGF receptor signaling reduces myofibroblast number and attenuates renal fibrosis

Valerie LeBleu; Raghu Kalluri

doi:10.1038/ki.2011.300

Blockade of PDGF receptor signaling reduces myofibroblast number and attenuates renal fibrosis

Valerie LeBleu, Raghu Kalluri

Cancer Biology

Research output: Contribution to journal › Comment/debate › peer-review

29 Scopus citations

Abstract

Fibrosis can be considered as wound healing that never ceases, and activated fibroblasts (myofibroblasts) probably play a critical role in this unabated tissue repair process. In the setting of renal fibrosis, two central questions remain unanswered: Where do activated myofibroblasts come from; and what mechanism or mechanisms keep them activated? The study by Chen and colleagues addresses the role of platelet-derived growth factor receptor (PDGFR) signaling in the activation of myofibroblasts.

Original language	English (US)
Pages (from-to)	1119-1121
Number of pages	3
Journal	Kidney International
Volume	80
Issue number	11
DOIs	https://doi.org/10.1038/ki.2011.300
State	Published - Dec 2011

ASJC Scopus subject areas

Nephrology

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10.1038/ki.2011.300

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title = "Blockade of PDGF receptor signaling reduces myofibroblast number and attenuates renal fibrosis",

abstract = "Fibrosis can be considered as wound healing that never ceases, and activated fibroblasts (myofibroblasts) probably play a critical role in this unabated tissue repair process. In the setting of renal fibrosis, two central questions remain unanswered: Where do activated myofibroblasts come from; and what mechanism or mechanisms keep them activated? The study by Chen and colleagues addresses the role of platelet-derived growth factor receptor (PDGFR) signaling in the activation of myofibroblasts.",

author = "Valerie LeBleu and Raghu Kalluri",

note = "Funding Information: The work of the authors is supported by a Research Training Grant in Gastroenterology (2T32DK007760-11) at Beth Israel Deaconess Medical Center, as well as by US National Institutes of Health grants DK055001, DK081576, and CA125550 and funds from the Department of Medicine to the Division of Matrix Biology at Beth Israel Deaconess Medical Center.",

year = "2011",

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T1 - Blockade of PDGF receptor signaling reduces myofibroblast number and attenuates renal fibrosis

AU - LeBleu, Valerie

AU - Kalluri, Raghu

N1 - Funding Information: The work of the authors is supported by a Research Training Grant in Gastroenterology (2T32DK007760-11) at Beth Israel Deaconess Medical Center, as well as by US National Institutes of Health grants DK055001, DK081576, and CA125550 and funds from the Department of Medicine to the Division of Matrix Biology at Beth Israel Deaconess Medical Center.

PY - 2011/12

Y1 - 2011/12

N2 - Fibrosis can be considered as wound healing that never ceases, and activated fibroblasts (myofibroblasts) probably play a critical role in this unabated tissue repair process. In the setting of renal fibrosis, two central questions remain unanswered: Where do activated myofibroblasts come from; and what mechanism or mechanisms keep them activated? The study by Chen and colleagues addresses the role of platelet-derived growth factor receptor (PDGFR) signaling in the activation of myofibroblasts.

AB - Fibrosis can be considered as wound healing that never ceases, and activated fibroblasts (myofibroblasts) probably play a critical role in this unabated tissue repair process. In the setting of renal fibrosis, two central questions remain unanswered: Where do activated myofibroblasts come from; and what mechanism or mechanisms keep them activated? The study by Chen and colleagues addresses the role of platelet-derived growth factor receptor (PDGFR) signaling in the activation of myofibroblasts.

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Blockade of PDGF receptor signaling reduces myofibroblast number and attenuates renal fibrosis

Abstract

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