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Tat depletes NO by reducing both endothelial nitric oxide synthase (eNOS) expression ( Figure 1 ) and NO production, thereby impairing endothelium-dependent vasorelaxation ( Figure 1 ) ( In another study, HIV-Tat exposure significantly increased endothelial cell senescence by upregulating miR-34a and downregulating miR-146a, which could promote the vascular infiltration of immune cells and the development of atherosclerotic vascular disease ( Table 1 )

GPX4, ferroptosis, and diseases

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Kwiatkowski, T

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Role of Epigenetic Modulation in Neurodegenerative Diseases: Implications of Phytochemical Interventions