Artificial intelligence has identified a gene capable of turning back the aging clock. Harvard Medical School researchers discovered that administering the SRSF1 gene to aged mice extended lifespan by 14% and slowed frailty progression by 44%. The approach is being hailed as a breakthrough that overcomes the limitations of existing cellular reprogramming techniques by inducing rejuvenation while preserving cells’ intrinsic functions.<\/p>\n
A research team led by Professor George M. Church of Harvard Medical School’s Department of Genetics published the findings on the 14th in the international journal Nature Aging. The international collaboration included Dr. Alexandru Plesa of the Wyss Institute.<\/p>\n
The study’s starting point was the cellular reprogramming technology developed by Professor Shinya Yamanaka of Japan’s Kyoto University, which earned him the 2012 Nobel Prize in Physiology or Medicine. That approach\u2014reverting mature cells to induced pluripotent stem cells (iPS cells)\u2014carried inherent problems: cells lost their original function and morphology during the reset to an immature state, and cancer risk increased significantly.<\/p>\n
The Harvard team took a different path. To identify genes capable of reversing aging without destroying cellular identity, they first built an “age-prediction model.” They trained machine learning algorithms on gene expression data from 464 human skin fibroblast samples collected across various age groups, enabling the model to accurately calculate “transcriptomic age”\u2014a numerical measure of age based on gene activity levels within cells.<\/p>\n
Using this model, the team conducted large-scale screening of key candidate genes involved in the aging process. The approach involved identifying genes whose overexpression could rejuvenate the transcriptomic age of senescent fibroblasts.<\/p>\n
SRSF1 Simultaneously Improves Three Major Hallmarks of Aging<\/p>\n
The screening identified SRSF1 as the gene with the most promising predicted rejuvenation effects. Activating this gene reactivated DNA repair programs in aged cells. Simultaneously, it reduced all major hallmarks of aging: “zombie cell” formation\u2014where damaged cells refuse to die and instead secrete inflammatory substances\u2014proteostatic stress from accumulated misfolded proteins, and chronic inflammation.<\/p>\n
Notably, cells maintained their original morphology and function throughout the rejuvenation process. Cancer risk did not increase either. This stands in stark contrast to Yamanaka’s reprogramming technique, which stripped cells of their identity by reverting them to an immature state.<\/p>\n
SRSF1’s mechanism of action lies in RNA splicing. The gene functions as an RNA splicing factor that precisely joins “alternative exons”\u2014specific segments required when messenger RNA (mRNA), the blueprint for protein production, is assembled. In essence, it helps aged cells properly express the optimal proteins needed for cellular repair and vitality maintenance.<\/p>\n
Lifespan Extended by 14% in Mouse Experiments<\/p>\n
The research team moved beyond cell experiments to validate efficacy in animal models. They loaded SRSF1 into a liver-tropic adeno-associated virus (AAV) and administered it to aged mice. Despite the gene being delivered primarily to the liver, anti-aging effects manifested throughout the entire body.<\/p>\n
Mice receiving SRSF1 showed a 44% slower frailty progression compared to controls, and median survival time increased by 14%. The rejuvenation of liver tissue slowed systemic frailty progression. The researchers hypothesize that changes originating in the liver may have influenced aging in other organs as well.<\/p>\n
Key experimental results are summarized below:<\/p>\n
MetricSRSF1 Treatment GroupControl GroupMedian survival time14% extensionBaselineFrailty progression rate44% slowerBaselineCell morphology & functionPreserved\u2014Cancer riskNot increased\u2014<\/p>\n
Note: Figures represent relative changes reported by the research team<\/p>\n
“We have opened a path to reversing aging by combining genetics with AI-based approaches,” the researchers stated. “We will continue to develop technologies for safely delivering SRSF1 to organs and tissues for future clinical applications.” They added, “Extending healthspan by modulating the activity of specific genes in aged tissues has been a long-standing research goal. This discovery represents a significant step toward that objective.”<\/p>\n
This study represents an early-stage investigation using cultured human cells and mice. Applying the findings to humans will require additional technologies to safely deliver the gene to target tissues and precisely regulate its activation level. The long-term safety of AAV vectors and potential side effects from SRSF1 overexpression remain subjects for follow-up research.<\/p>\n
The field of “rejuvenation medicine”\u2014treating aging as a disease\u2014has accelerated with the introduction of AI technologies. Whereas researchers previously formulated hypotheses and validated genes one by one, machine learning-based large-scale candidate screening, as demonstrated in this study, has dramatically expanded the scope of exploration. The discovery opens the possibility of identifying additional genes beyond SRSF1 that contribute to age reversal.<\/p>\n","protected":false},"excerpt":{"rendered":"Artificial intelligence has identified a gene capable of turning back the aging clock. Harvard Medical School researchers discovered…\n","protected":false},"author":2,"featured_media":930298,"comment_status":"","ping_status":"","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[7],"tags":[18538,64,63,52560,160358,92537,496988,496990,128,496989,496987,496991],"class_list":["post-930297","post","type-post","status-publish","format-standard","has-post-thumbnail","category-science","tag-adeno-associated-virus","tag-au","tag-australia","tag-george-church","tag-harvard-medical-school","tag-induced-pluripotent-stem-cells","tag-nature-aging","tag-rna-splicing","tag-science","tag-shinya-yamanaka","tag-srsf1","tag-transcriptomic-age"],"_links":{"self":[{"href":"https:\/\/www.newsbeep.com\/au\/wp-json\/wp\/v2\/posts\/930297","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.newsbeep.com\/au\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/www.newsbeep.com\/au\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/www.newsbeep.com\/au\/wp-json\/wp\/v2\/users\/2"}],"replies":[{"embeddable":true,"href":"https:\/\/www.newsbeep.com\/au\/wp-json\/wp\/v2\/comments?post=930297"}],"version-history":[{"count":0,"href":"https:\/\/www.newsbeep.com\/au\/wp-json\/wp\/v2\/posts\/930297\/revisions"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/www.newsbeep.com\/au\/wp-json\/wp\/v2\/media\/930298"}],"wp:attachment":[{"href":"https:\/\/www.newsbeep.com\/au\/wp-json\/wp\/v2\/media?parent=930297"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/www.newsbeep.com\/au\/wp-json\/wp\/v2\/categories?post=930297"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/www.newsbeep.com\/au\/wp-json\/wp\/v2\/tags?post=930297"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}