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

TL;DR

This paper reviews how drugs targeting TEC family kinases can cause cardiovascular side effects and explores the mechanisms behind these effects.

Contribution

The paper provides the first comprehensive review of cardiovascular toxicity associated with TEC family kinase inhibitors.

Findings

TEC family kinases are linked to various cardiovascular diseases.

Inhibitors of these kinases show cardiovascular toxicity through multiple molecular mechanisms.

Toxicity varies across different TEC family kinase inhibitors and drug generations.

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.

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