TAK1 in Vascular Signaling: “Friend or Foe”?

Abstract

The maintenance of normal vascular function and homeostasis is largely dependent on the signaling mechanisms that occur within and between cells of the vasculature. TGF-β-activated kinase 1 (TAK1), a multifaceted signaling molecule, has been shown to play critical roles in various tissue types. Although the precise function of TAK1 in the vasculature remains largely unknown, emerging evidence suggests its potential involvement in both physiological and pathological processes. A comprehensive search strategy was employed to identify relevant studies, PubMed, Web of Science, and other relevant databases were systematically searched using keywords related to TAK1, TABs and MAP3K7.In this review, we discussed the role of TAK1 in vascular signaling, with a focus on its function, activation, and related signaling pathways. Specifically, we highlight the TA1-TABs complex is a key factor, regulating vascular smooth muscle cells (VSMCs) and endothelial cells (ECs) involved in the processes of inflammation, vascular proliferation and angiogenesis. This mini review aims to elucidate the evidence supporting TAK1 signaling in the vasculature, in order to better comprehend its beneficial and potential harmful effects upon TAK1 activation in vascular tissue.

Keywords:

• TGF-β-activated kinase 1
• vascular disease
• mitogen-activated protein kinase
• transforming growth factor-β
• smooth muscle cell
• endothelial cell

Author Contributions

Gang Fan, Jingfen Lu and Jinhui Zha share first authorship. All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Disclosure

The authors report no conflicts of interest in this work.

Additional information

Funding

GF is supported by the National Natural Science Foundation of China (82001489), Shenzhen Natural Science Foundation (JCYJ 20220530141613031), Shenzhen Nanshan District Science and Technology Plan Project (NS044), Huazhong University of Science and Technology Union Shenzhen Hospital Foundation. Weiming Guo is supported by the Health Bureau of Nanshan District, Shenzhen (NSZD2023010) and Shenzhen Natural Science Foundation (JCYJ20230807115817037).