A recently published paper from the scripps research institute florida, has found a novel role for the tumor suppressor gene, spns1, in senescence, and omeprazole can compensate for a deficiency in spns1 expression, indicating a mechanistic interaction.
"The new study shows that Spns1, in conjunction with another pair of tumor suppressor genes, beclin 1 and p53 can, influences developmental senescence through two differential mechanisms: the Spns1 defect was enhanced by Beclin 1 but suppressed by basal p53. In addition to affecting senescence, Spns1 impedes autophagy, the process whereby cells remove unwanted or destructive proteins and balance energy needs during various life stages.
"Building on their insights from the study, Kishi and his colleagues noted in the future therapeutics might be able influence aging through Spns1. He noted one commonly used antacid, Prilosec, has been shown to temporarily suppress autophagic abnormality and senescence observed in the Spns1 deficiency."
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