韓國媒體報(bào)道，韓國成均館大學(xué)醫(yī)學(xué)院分子細(xì)胞生物學(xué)教室的申在均（音譯）教授團(tuán)隊(duì)今天表示,，透過老鼠實(shí)驗(yàn),，發(fā)現(xiàn)若缺乏名為p62的基因，則細(xì)胞內(nèi)粒腺體的功能會衰弱,，使得快速老化,。
研究團(tuán)隊(duì)證實(shí)，正常老鼠的壽命越老時(shí),，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(tuán)隊(duì)表示,，p62基因能穩(wěn)定名為Nrf2的轉(zhuǎn)錄因子（transcription factor），使名為Nqo1的抗氧化酵素維持在一定水準(zhǔn),，結(jié)果會導(dǎo)致細(xì)胞內(nèi)氧化物質(zhì)減少并抑制老化,。
研究團(tuán)隊(duì)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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PMID:
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.
