Table 1.
The expression and function of TSPs in cardiovascular cells under distinct mechanical stimuli
| Pathological States | Expression Tissue/Cell Type | Mechanical Stimulus | Name of TSPs | TSPs Function | Ref. |
|---|---|---|---|---|---|
| Vascular regenerative repair | Endothelial cells (ECs) | Laminar shear stress (6–15 dyn/cm²) | TSP-1↓ | Shear stress downregulates TSP-1/CD36, reducing EC apoptosis and promoting vascular homeostasis | [56, 57] |
| Atherosclerosis | Endothelial cells (ECs) | Disturbed flow (low/oscillatory shear) | TSP-1↑ | Upregulated TSP-1 activates TGF-β-dependent fibrotic pathways (COL1A1, CTGF, PAI1↑) | [46] |
| Pulmonary hypertension (PH) | Pulmonary artery endothelial cells (PAECs) | Tensile force | TSP-1↑ | Inhibiting PAEC proliferation via CD36/CD47 binding | [27] |
| Vascular remodeling | Vascular smooth muscle cells (SMCs) | Cyclic tensile stress | TSP-1↑ | Stabilizing F-actin complexes, enhancing cellular rigidity, and inhibiting SMC proliferation | [61] |
| Diabetic/ Hypertensive myopathy | Myocardial tissue | Pressure overload | TSP-1↑ | Promoting myocardial fibrosis via TGF-β activation and exacerbating injury | [47] |
| Pulmonary vascular remodeling | Pulmonary arterial smooth muscle cells (PASMCs) | Pathological pressure | TSP-1↑ | Enhancing ER stress via JAK2-STAT3-TSP-1, driving PASMC proliferation/migration | [69] |
| Aortic pressure overload | Aortic vasculature | Transverse aortic constriction (TAC) | TSP-2↑ | Preserving vascular structural integrity; deficiency causes medial-adventitial separation | [70] |
| Cardiac hypertrophy | Myocardium | Pressure overload | TSP-4↑ | Mitigating cardiomyocyte injury/fibrosis by modulating ER stress responses | [71, 35] |
| Right ventricular pressure overload | Right ventricular cardiomyocytes | Pressure overload | TSP-4↑ | Suppressing hypertrophy/fibrosis via JNK/Runx2 signaling | [72] |