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疼痛感觉与死亡率增加有关,但是痛觉是否直接影响老化尚未可知。美国科学家Riera等发现,TRPV1疼痛受体缺失的小鼠会变得长寿,在老年阶段呈现出年轻的代谢状态。TRPV1的缺失能阻止钙信号的级联反应,这种钙信号级联反应终止于脊髓痛觉神经元中由CREB调节的转录共激活因子CRTC1的核输出。在长寿的TRPV1基因敲除小鼠,CRTC1的核输出降低了神经肽降钙素基因相关肽(calcitonin gene-related peptide,CGRP;来自支配胰岛的感觉神经末梢)的产量,随后促进胰岛素的
Pain sensation is associated with increased mortality, but it is not yet known whether the pain sensation affects aging directly. American scientist Riera et al found that mice deficient in the TRPV1 pain receptor can become longevity and exhibit a young metabolic state in the elderly. Deletion of TRPV1 prevents the cascade of calcium signaling that terminates in the nuclear export of CREB-regulated transcriptional coactivator CRTC1 in spinal pain neurons. In long-lived TRPV1 knockout mice, nuclear export of CRTC1 decreases the production of the neuropeptide calcitonin gene-related peptide (CGRP; from the sensory nerve endings that govern the islets), followed by the promotion of insulin