韩国媒体报道，韩国成均馆大学医学院分子细胞生物学教室的申在均（音译）教授团队今天表示，透过老鼠实验，发现若缺乏名為p62的基因，则细胞内粒腺体的功能会衰弱，使得快速老化。
研究团队证实，正常老鼠的寿命越老时，p62基因就会急遽减少，p62基因功能越衰弱，就越无法抑制老化。
研究团队表示，p62基因能稳定名為Nrf2的转录因子（transcription factor），使名为Nqo1的抗氧化酵素维持在一定水準，结果会导致细胞内氧化物质减少并抑制老化。
研究团队期盼此次研究能有助於日后开发人类抗老化的药物。(生物谷 Bioon.com)
doi:10.1038/embor.2011.246
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Assurance of mitochondrial integrity and mammalian longevity by the p62–Keap1–Nrf2–Nqo1 cascade
Jeongho Kwon, Eunhye Han, Chi-Bao Bui, Woochul Shin, Junho Lee, Sejeong Lee, Young-Bong Choi, Ann-Hwee Lee, Kyong-Hoon Lee, Chankyu Park, Martin S Obin, Sung Kyu Park, Yun Jeong Seo, Goo Taeg Oh, Han-Woong Lee & Jaekyoon Shin
Sqstm1/p62 functions in the non-canonical activation of nuclear factor (erythroid-derived 2)-like 2 (Nrf2). However, its physiological relevance is not certain. Here, we show that p62 −/− mice exhibited an accelerated presentation of ageing phenotypes, and tissues from these mice created a pro-oxidative environment owing to compromised mitochondrial electron transport. Accordingly, mitochondrial function rapidly declined with age in p62 −/− mice. In addition, p62 enhanced basal Nrf2 activity, conferring a higher steady-state expression of NAD(P)H dehydrogenase, quinone 1 (Nqo1) to maintain mitochondrial membrane potential and, thereby, restrict excess oxidant generation. Together, the p62–Nrf2–Nqo1 cascade functions to assure mammalian longevity by stabilizing mitochondrial integrity.
