韓國媒體報道,，韓國成均館大學醫(yī)學院分子細胞生物學教室的申在均（音譯）教授團隊今天表示,，透過老鼠實驗，發(fā)現若缺乏名為p62的基因,，則細胞內粒腺體的功能會衰弱，使得快速老化,。
研究團隊證實,，正常老鼠的壽命越老時，p62基因就會急遽減少,，p62基因功能越衰弱，就越無法抑制老化,。
研究團隊表示，p62基因能穩(wěn)定名為Nrf2的轉錄因子（transcription factor）,，使名為Nqo1的抗氧化酵素維持在一定水準，結果會導致細胞內氧化物質減少并抑制老化,。
研究團隊期盼此次研究能有助於日后開發(fā)人類抗老化的藥物。(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.
