Methionine restriction, i.e., a partial depletion of the essential sulfur amino acid methionine from nutrition, extends lifespan in model organisms including yeast, nematodes, mice and rats. Recent results indicate that this strategy also prolongs health span and longevity in 2 short-lived strains of mice (with the LmnaG609G/G609G or zmpste24-/- genotypes) that represent animal models of Hutchinson-Gilford progeria syndrome (HGPS). The beneficial effects of methionine restriction on HGPS could be linked to reduced inflammation, and improved DNA stability, as well as the normalization of lipid and bile acid metabolism. Previous work has established that behavioral, nutritional, pharmacological and genetic manipulations that extend longevity in model organisms are only efficient if they induce increased autophagic flux. Methionine restriction extends lifespan in Saccharomyces cerevisiae in an Atg5- and Atg7-dependent fashion, supporting the notion that methionine restriction may indeed mediate its antiaging effects through the induction of macroautophagy/autophagy as well. Based on these findings, we speculate that autophagy might constitute an actionable therapeutic target to treat progeroid syndromes.

中文翻译：

---

限制蛋氨酸改善早衰：另一种自噬诱导的抗衰老策略？

蛋氨酸的限制，即营养中必需硫氨基酸蛋氨酸的部分消耗，延长了模型生物的寿命，包括酵母，线虫，小鼠和大鼠。最近的结果表明，该策略还可以延长代表Hutchinson-Gilford早衰综合征（HGPS）动物模型的2种短寿命小鼠品系（具有LmnaG609G / G609G或zmpste24-/-基因型）的健康寿命和寿命。限制蛋氨酸对HGPS的有益作用可能与减少炎症，改善DNA稳定性以及脂质和胆汁酸代谢正常化有关。先前的工作已经确定，延长模型生物寿命的行为，营养，药理和基因操作只有在诱导自噬通量增加的情况下才有效。蛋氨酸限制以Atg5和Atg7依赖的方式延长了酿酒酵母的寿命，支持了蛋氨酸限制确实可以通过诱导巨自噬/自噬来介导其抗衰老作用的观点。基于这些发现，我们推测自噬可能构成了治疗早衰综合症的可行治疗靶标。