Vascular smooth muscle cell proliferation as a therapeutic target. Part 1: molecular targets and pathways

Cardiovascular diseases are a major cause of human death worldwide. Excessive proliferation of vascular smooth muscle cells contributes to the etiology of such diseases, including atherosclerosis, restenosis, and pulmonary hypertension. The control of vascular cell proliferation is complex and encom...

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Bibliographic Details
Published in:	Biotechnology advances Vol. 36; no. 6; pp. 1586 - 1607
Main Authors:	Wang, Dongdong, Uhrin, Pavel, Mocan, Andrei, Waltenberger, Birgit, Breuss, Johannes M., Tewari, Devesh, Mihaly-Bison, Judit, Huminiecki, Łukasz, Starzyński, Rafał R., Tzvetkov, Nikolay T., Horbańczuk, Jarosław, Atanasov, Atanas G.
Format:	Journal Article
Language:	English
Published:	England Elsevier Inc 01.11.2018 Elsevier Science Ltd
Subjects:	Atherosclerosis Cancer Cardiovascular diseases Cascades Cell cycle cell proliferation Etiology Heart diseases Hypertension Lead compounds Muscles myocytes Natural products Proliferation Pulmonary hypertension Restenosis signal transduction Signaling Signaling pathway Smooth muscle therapeutics Therapy Vascular endothelial growth factor Vascular smooth muscle cells LMW-DSP2 eNOS NRG CDK INK4 AP-1 DEP-1 IGF1R PI3K SHIP PPAR-γ PDK1 IP3R1 IL TRAIL STATs PLA2 IR SERCA BMPR-II bFGF CVD SHP-2 PBEF Pyk2 GPCR VSMC IRE P70S6K SIRT ERK HDAC DRP-1 TNF-R1 RTK IRS cAMP Rb TRPM2 CREB Signaling pathway TERT Cell cycle PDGFR miRNA TGF-β MKKK Vascular smooth muscle cells SR GLUT1 Cip/Kip ACE BMP SOCS-3 PGC-1α PP2A DAG MKK Pulmonary hypertension Ang II ECM PAH Grb2 SH2 CaMK JNK PTEN aFGF NF-κB IFN-γ TRP mTOR HSG EC AT-1R FGF Tyk2 PKB PKA PLC-γ PKC IGF-1 MAPK ER PKG Restenosis ET-1 NOS Nox ROS PIP3 Cardiovascular diseases PTA mTORC1 Sos1 PIP2 Bcl-2 NADPH NO PCNA LRP1 Sp-1 cGMP PLD GSK-3 SHP-1 PTP EGFR NFAT IκB PDE LDL Atherosclerosis UCP2 Mfn2 GF CKI WTAP EGF ASK1 MMPs Proliferation LMW-PTP IP3 NAD FAK DES TNF-α JAK WT1 PDGF LMW
ISSN:	0734-9750, 1873-1899, 1873-1899
Online Access:	Get full text
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