由希伯来大学的Dr. Marva Bergman和Prof. Itamar Harel领导的国际研究团队发现，免疫系统的过度反应可能是导致某些遗传性衰老疾病加速衰老的关键因素1。当DNA片段泄漏到细胞错误部位时，免疫传感器cGAS会误将其识别为病毒感染信号，从而触发慢性炎症并干扰DNA修复过程1。这一"假警报"机制在共济失调毛细血管扩张症和布鲁姆综合征等DNA损伤修复综合征中尤为显著1。
研究团队通过降低cGAS活性的方式进行干预，在多个生物系统中实现了显著改善1。这些改善包括减轻神经炎症、逆转组织退化以及恢复生殖能力1。cGAS在驱动衰退的过程中发挥双重作用——既促进炎症反应，又干扰关键的DNA修复分子1。该研究成果已于2026年9月16日发表在《Genes》杂志第40卷第11-12期，页码852，研究团队与南加州大学开展了合作1。
An international research team led by Hebrew University has uncovered a mechanism in which the immune system's overreaction to misplaced DNA fragments may accelerate aging in certain genetic disorders. 1 When DNA segments leak into incorrect cellular locations, the immune sensor cGAS mistakenly interprets this as a viral infection signal, triggering chronic inflammation and disrupting the cell's ability to repair DNA damage. 1 By reducing cGAS activity, researchers were able to improve tissue function across multiple biological systems. 1
The study focused on DNA damage repair (DDR) syndromes, including ataxia-telangiectasia (A-T) and Bloom syndrome. 1 The research, led by Dr. Marva Bergman and Prof. Itamar Harel at Hebrew University in collaboration with the University of Southern California, demonstrated that cGAS drives disease progression in two distinct ways: by promoting inflammation and by interfering with DNA repair molecules. 1 Lowering cGAS activity reversed several hallmark features of these conditions, including neuroinflammation, tissue degeneration, and loss of reproductive capacity. 1 The findings were published in Genes magazine in September 2026. 1
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