Advancements in research on the cardiovascular toxicity caused by TEC family kinases inhibitors

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Authors: Y. S. Zhang, Huangxi Fu, Xingchen Kang, Zixuan Qiu, Hao Yan, Qiaojun He, Bo Yang, Zhifei Xu, Peihua Luo
Cited by: 3
References: 117

Abstract

The tyrosine kinase expressed in hepatocellular carcinoma (TEC) family kinases (TFKs) are a subfamily of non-receptor protein tyrosine kinases (PTKs) that include five members: TEC, bruton's tyrosine kinase (BTK), interleukin 2-inducible T-cell kinase (ITK/EMT/TSK), bone marrow tyrosine kinase on chromosome X (BMX/ETK), and tyrosine-protein kinase (TXK/RLK). They play key roles in cell signaling and immune regulation. Emerging evidence highlights their involvement in cardiovascular diseases (CVDs) such as ischemic heart disease (IHD), atherosclerosis (AS), sepsis-related dysfunction, atrial fibrillation (AF), myocardial hypertrophy, coronary atherosclerotic heart disease, myocardial infarction (MI), and post-myocardial infarction complications. However, no review has comprehensively addressed the cardiovascular toxicity of TFKs inhibitors. This review provides a comprehensive and systematic analysis of the cardiovascular toxicity profiles of TFK inhibitors (TFKis), focusing on underlying molecular mechanisms, comparing toxicity across different agents and generations, and discussing clinical implications.

Fields of Study & Subjects

PI3K/AKT/mTOR signaling in cancer Metabolism Diabetes and Cancer Chronic Lymphocytic Leukemia Research

Publication details

Journal / source
Frontiers in Pharmacology
Publisher
Frontiers Media SA
Volume
16
Pages
1726458–1726458
Publication date
6 January 2026
Language
EN