Table 2.
The Tec family kinases functions and regulation.
| Kinase | Mechanisms | Biological response | References |
|---|---|---|---|
| TEC | Ischemic injury as well as purines can stimulate Tec kinase translocation in cardiomyocytes. Tec regulates proteins associated with lipid membranes, and is involved in the temporal response of the heart to ischemia-reperfusion. | Ischaemic heart disease | [33, 34] |
| Tec may play a cardioprotective role by binding to ROCK1. | Cardiac pressure overload hypertrophy | [33, 35] | |
| BTK | BTK promotes ox-LDL-induced ER stress, oxidative stress, and inflammatory responses in macrophages, and BTK knockdown can inhibit ox-LDL-induced B signaling activation and inhibit M1 polarization in NK-κ macrophages.BTK regulates the NLRP3 inflammasome.Btk is involved in bt/VWF (Botrocetin/von Willebrand factor) -mediated lectin-induced TxA2 production and GPIb-dependent arterial thrombosis. | Atherosclerosis | [41–56] |
| Btk plays a role in Toll-like receptor signaling and NLRP3 inflammasome activation. | Sepsis-related cardiac dysfunction | [46, 47, 57, 68] | |
| BTK promotes NLRP3 inflammasome activation. | Atrial fibrillation | [46, 47, 69] | |
| BMX | The effect of Bmx on cardiac hypertrophy is mediated through the endothelial cells of the coronary vessels. | Cardiac hypertrophy | [73, 77] |
| Bmx regulates VEGFR2 expression and VEGF-induced angiogenesis, and Bmx is also a downstream effector of VEGFR2. It is involved in ischemia-induced arteriogenesis and angiogenesis. Bmx is also involved in cell adhesion, migration and survival in TNF-induced angiogenesis. | Coronary atherosclerotic heart disease | [78–83] | |
| Bmx is involved in the mechanism of NO-induced PKC-ε signaling and VEGF-dependent lymphangiogenesis signaling. | Myocardial Infarction and Post-Myocardial Infarction | [84–87] | |
| ITK | None | None | None |
| TXK | None | None | None |