University of Tasmania
Browse
- No file added yet -

TAK1 signaling is a potential therapeutic target for pathological angiogenesis

Download (2.4 MB)
journal contribution
posted on 2023-05-20, 22:17 authored by Zhu, L, Lama, S, Tu, L, Dusting, GJ, Wang, J-H, Guei-Sheung LiuGuei-Sheung Liu
Angiogenesis plays a critical role in both physiological responses and disease pathogenesis. Excessive angiogenesis can promote neoplastic diseases and retinopathies, while inadequate angiogenesis can lead to aberrant perfusion and impaired wound healing. Transforming growth factor β activated kinase 1 (TAK1), a member of the mitogen-activated protein kinase kinase kinase family, is a key modulator involved in a range of cellular functions including the immune responses, cell survival and death. TAK1 is activated in response to various stimuli such as proinfammatory cytokines, hypoxia, and oxidative stress. Emerging evidence has recently suggested that TAK1 is intimately involved in angiogenesis and mediates pathogenic processes related to angiogenesis. Several detailed mechanisms by which TAK1 regulates pathological angiogenesis have been clarifed, and potential therapeutics targeting TAK1 have emerged. In this review, we summarize recent studies of TAK1 in angiogenesis and discuss the crosstalk between TAK1 and signaling pathways involved in pathological angiogenesis. We also discuss the approaches for selectively targeting TAK1 and highlight the rationales of therapeutic strategies based onTAK1 inhibition for the treatment of pathological angiogenesis.

Funding

National Health & Medical Research Council

History

Publication title

Angiogenesis

ISSN

0969-6970

Department/School

Menzies Institute for Medical Research

Publisher

Springer Netherlands

Place of publication

Netherlands

Rights statement

© The Author(s), under exclusive licence to Springer Nature B.V. 2021. Post-prints are subject to Springer Nature re-use terms

Repository Status

  • Restricted

Socio-economic Objectives

Treatment of human diseases and conditions; Expanding knowledge in the biomedical and clinical sciences

Usage metrics

    University Of Tasmania

    Exports

    RefWorks
    BibTeX
    Ref. manager
    Endnote
    DataCite
    NLM
    DC