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TBX3 played a key role in regulating cellular senescence by repressing p14 ARF expression through interactions with histone deacetylases (HDACs), and by inhibiting p16 INK4a either through suppression of cyclin-dependent kinase activity or by cooperating with the polycomb protein EZH2 to promote its epigenetic silencing [45, 46]

These findings reinforce the clinical evidence that ASD is associated with an abnormal inflammatory response

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Shi Y, Chen J, Li S, et al

GSTs, in turn, conjugate GSH to xenobiotics in a first step of detoxification 53,54

This relationship was also significant for each patient subgroup individually (hypertensives: r =0.64, P =0.002