時(shí)光一天天地逝去,，人們慢慢地變老，其中的過程對(duì)人類來說是個(gè)巨大的謎題,。德國科學(xué)家近日鑒別出一組蛋白,，能夠揭示一個(gè)人的生物學(xué)年齡。這些生物標(biāo)記可應(yīng)用于醫(yī)學(xué)之中,，根據(jù)老年人的個(gè)體生物學(xué)年齡改進(jìn)對(duì)他們的治療,。相關(guān)論文發(fā)表在美國《國家科學(xué)院院刊》（PNAS）上。
隨著生活條件和醫(yī)療條件的日益改善,，人類的壽命在不斷延長,。但是同時(shí)，很多老年人遭受著年齡相關(guān)性疾病的煎熬,，而且由于實(shí)足年齡（chronological age）不一定與生物學(xué)年齡相符,，醫(yī)生們經(jīng)常很難決定使用哪種治療手段。
在最新的研究中,，德國馬普干細(xì)胞老化研究所的Lenhard Rudolph和同事仔細(xì)研究了端粒,。端粒位于染色體末端，能保持染色體穩(wěn)定,，并起到保護(hù)作用,。然而，細(xì)胞每次分裂,，端粒都會(huì)縮短50至200個(gè)堿基對(duì),。在人體老化的過程中，端粒變得越來越短直至喪失了保護(hù)功能,。結(jié)果,，染色體變得不穩(wěn)定，細(xì)胞喪失了分裂能力,?？茖W(xué)家認(rèn)為這就是細(xì)胞老化的原因之一,。
Rudolph和同事發(fā)現(xiàn)，端粒的縮短和DNA損傷會(huì)在人類細(xì)胞中造成重疊反應(yīng),。在這兩種情況中,，受影響的細(xì)胞會(huì)釋放標(biāo)記蛋白。Rudolph說：“令人感興趣的是,，同一種蛋白能在人類血液中檢測(cè)到,，而且其量的明顯增加與衰老及年齡相關(guān)性疾病有關(guān)。”
這一研究結(jié)果不僅為生物學(xué)年齡提供了有意義的標(biāo)記,，同時(shí)也確證了人類衰老的DNA損傷假說,。研究人員希望這些標(biāo)記能在醫(yī)療中得到應(yīng)用，這將使根據(jù)病患個(gè)體生物學(xué)年齡改進(jìn)治療成為可能,，從而達(dá)到更好的效果,。此外，Rudolph認(rèn)為還有其它的應(yīng)用,。他說：“它們也可被用于測(cè)試行為干預(yù),、食品添加劑及藥物治療，以延緩老化過程,。”（生物谷Bioon.com）
生物谷推薦原始出處：
PNAS,，vol. 105 no. 32 11299-11304，Hong Jianga,，K. Lenhard Rudolpha
Proteins induced by telomere dysfunction and DNA damage represent biomarkers of human aging and disease
Hong Jianga,b, Eric Schifferc, Zhangfa Songa, Jianwei Wanga, Petra Zürbigc, Kathrin Thedieckd, Suzette Moesd, Heike Bantele, Nadja Saale, Justyna Jantosc, Meiken Brechtf, Paul Jen?d, Michael N. Halld, Klaus Hagerf, Michael P. Mannse, Hartmut Heckerg, Arnold Ganserh, Konstanze D?hneri, Andrzej Bartkej, Christoph Meissnerk, Harald Mischakc, Zhenyu Jua,l, and K. Lenhard Rudolpha,m
Abstract
Telomere dysfunction limits the proliferative capacity of human cells by activation of DNA damage responses, inducing senescence or apoptosis. In humans, telomere shortening occurs in the vast majority of tissues during aging, and telomere shortening is accelerated in chronic diseases that increase the rate of cell turnover. Yet, the functional role of telomere dysfunction and DNA damage in human aging and diseases remains under debate. Here, we identified marker proteins (i.e., CRAMP, stathmin, EF-1α, and chitinase) that are secreted from telomere-dysfunctional bone-marrow cells of late generation telomerase knockout mice (G4mTerc−/−). The expression levels of these proteins increase in blood and in various tissues of aging G4mTerc−/− mice but not in aging mice with long telomere reserves. Orthologs of these proteins are up-regulated in late-passage presenescent human fibroblasts and in early passage human cells in response to γ-irradiation. The study shows that the expression level of these marker proteins increases in the blood plasma of aging humans and shows a further increase in geriatric patients with aging-associated diseases. Moreover, there was a significant increase in the expression of the biomarkers in the blood plasma of patients with chronic diseases that are associated with increased rates of cell turnover and telomere shortening, such as cirrhosis and myelodysplastic syndromes (MDS). Analysis of blinded test samples validated the effectiveness of the biomarkers to discriminate between young and old, and between disease groups (MDS, cirrhosis) and healthy controls. These results support the concept that telomere dysfunction and DNA damage are interconnected pathways that are activated during human aging and disease.
