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Review
. 2017 Dec;16(6):7879-7889.
doi: 10.3892/mmr.2017.7641. Epub 2017 Sep 27.

PDGF signaling pathway in hepatic fibrosis pathogenesis and therapeutics (Review)

Hua-Zhong Ying  1 , Qin Chen  2 , Wen-You Zhang  1 , Huan-Huan Zhang  1 , Yue Ma  1 , Song-Zhao Zhang  2 , Jie Fang  1 , Chen-Huan Yu  1
Affiliations
Review

PDGF signaling pathway in hepatic fibrosis pathogenesis and therapeutics (Review)

Hua-Zhong Ying et al. Mol Med Rep. 2017 Dec.

Abstract

The platelet‑derived growth factor (PDFG) signaling pathway exerts persistent activation in response to a variety of stimuli and facilitates the progression of hepatic fibrosis. Since this pathway modulates a broad spectrum of cellular processes, including cell growth, differentiation, inflammation and carcinogenesis, it has emerged as a therapeutic target for hepatic fibrosis and liver‑associated disorders. The present review exhibits the current knowledge of the role of the PDGF signaling pathway and its pathological profiles in hepatic fibrosis, and assesses the potential of inhibitors which have been investigated in the experimental hepatic fibrosis model, in addition to the clinical challenges associated with these inhibitors.

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Figures

Figure 1.
Figure 1.
Schematic representation of the PDGF signaling pathway. PDGF, platelet-derived growth factor; PDGFR, PDGF receptor; miR, microRNA; PI3K, phosphatidylinositol 3-kinase; PLCγ, phospholipase Cγ; Sos, son of sevenless homolog; JAK1, tyrosine-protein kinase JAK1; PDK1, 3-phosphoinositide-dependent protein kinase 1; Akt, RAC-α serine/threonine protein kinase; PTEN, phosphatidylinositol 3,4,5-trisphosphate 3-phosphatase and dual-specificity protein phosphatase PTEN; ROCK, Rho-associated protein kinase 1; MLC, membrane protein MLC; NF-κB, nuclear factor-κB; IKKα, inhibitor of NF-κB kinase subunit α; C/EBPβ, CCAAT/enhancer-binding protein β; STAT, signal transducer and activator of transcription; MEK, dual specificity mitogen-activated protein kinase kinase; Erk, extracellular signal-regulated kinase; AP-1, transcription factor AP-1; TIMP, metalloproteinase inhibitor; c-Myc, myc proto-oncogene protein; CT1, cardiotrophin 1.
Figure 2.
Figure 2.
Recent challenges and future strategies for the treatment of hepatic fibrosis.
See this image and copyright information in PMC

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