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Thyroid hormone-induced angiogenesis.

作者信息

Davis Paul J, Davis Faith B, Mousa Shaker A

机构信息

Ordway Research Institute, Inc., Albany, New York.

出版信息

Curr Cardiol Rev. 2009 Jan;5(1):12-6. doi: 10.2174/157340309787048158.

DOI:10.2174/157340309787048158
PMID:20066142
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2803282/
Abstract

A series of reports in the past decade have ascribed pro-angiogenic activity to several thyroid hormone analogues, including L-thyroxine (T(4)), 3,5,3-triiodo-L-thyronine (T(3)) and diiodothyropropionic acid (DITPA). Model systems of angiogenesis have demonstrated that thyroid hormone-induced neovascularization is initiated at a cell surface receptor for the hormone on an integrin. The hormone signal is transduced within the cell by extracellular regulated kinase 1/2 (ERK1/2) into secretion of basic fibroblast growth factor (bFGF) and other vascular growth factors and consequent angiogenesis. Intact animal studies have shown that endogenous thyroid hormone supports blood vessel density in heart and brain and that thyroid hormone administration can induce angiogenesis in ischemic limbs.

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a47/2803282/2c9957c27e8d/CCR-5-12_F1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a47/2803282/2c9957c27e8d/CCR-5-12_F1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a47/2803282/2c9957c27e8d/CCR-5-12_F1.jpg

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