Table 1.
References | Relevant risk factors | Main viewpoint |
---|---|---|
Jing et al. 2015[65] | SM22alpha promoter | In VSMC, the SM22alpha promoter, carried by a recombinant lentiviral vector, was used to successfully infect and selectively upregulate expression of p27 protein, which restrains intimal hyperplasia with inhibition of endothelial repair |
Wang et al. 2015[66] | SOCE | The decrease of SOCE led to EPC damage potentially by downregulating SOCC and impairing eNOS pathway |
Ostrowski et al. 2017[67] | Sympathoadrenal activation | Sympathoadrenal activation, injuring endothelial function, was dramatically correlative with hypocoagulability and endotheliopathy |
Rodríguez-Carrio et al. 2015[68] | RDW | RDW was related with endothelial progenitor cells consumption and incremental concentrations of various intermediaries connected to endothelial injury, thereby which unmask novel insight on the science of RDW as predictive factors |
Bochenek et al. 2016[69] | Aging | The damaged proliferation and migration of local endothelial cells as well as exhaustion of endogenous endothelial repair mechanisms become worse with age by impairing re-endothelialization |
Reynolds et al. 2016[70] | Deficiency of Vitamin D | Vitamin D shortage is associated with poor vascular repair and weakened endothelial function and may regulate inflammatory reaction |
VSMC: Vascular smooth muscle cells; EPC: Endothelial progenitor cell; SOCE: Store-operated calcium entry; SOCC: Store-operated calcium channel; eNOS: Endothelial nitric oxide synthase; RDW: Red cell distribution width.