کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8341398 | 1541424 | 2018 | 19 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
PDGF in organ fibrosis
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
Fibrosis is part of a tissue repair response to injury, defined as increased deposition of extracellular matrix. In some instances, fibrosis is beneficial; however, in the majority of diseases fibrosis is detrimental. Virtually all chronic progressive diseases are associated with fibrosis, representing a huge number of patients worldwide. Fibrosis occurs in all organs and tissues, becomes irreversible with time and further drives loss of tissue function. Various cells types initiate and perpetuate pathological fibrosis by paracrine activation of the principal cellular executors of fibrosis, i.e. stromal mesenchymal cells like fibroblasts, pericytes and myofibroblasts. Multiple pathways are involved in fibrosis, platelet-derived growth factor (PDGF)-signaling being one of the central mediators. Stromal mesenchymal cells express both PDGF receptors (PDGFR) α and β, activation of which drives proliferation, migration and production of extracellular matrix, i.e. the principal processes of fibrosis. Here, we review the role of PDGF signaling in organ fibrosis, with particular focus on the more recently described ligands PDGF-C and -D. We discuss the potential challenges, opportunities and open questions in using PDGF as a potential target for anti-fibrotic therapies.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular Aspects of Medicine - Volume 62, August 2018, Pages 44-62
Journal: Molecular Aspects of Medicine - Volume 62, August 2018, Pages 44-62
نویسندگان
Barbara Mara Klinkhammer, Jürgen Floege, Peter Boor,