Barthez Marine, Song Zehan, Feng Yufan, Wang Yifei, Wang Chih-Ling, Chen Danica
Department of Nutritional Sciences and Toxicology, University of California, Berkeley, California, USA.
Metabolic Biology Graduate Program, University of California, Berkeley, California, USA.
Aging Cell. 2025 Sep;24(9):e70162. doi: 10.1111/acel.70162. Epub 2025 Jul 4.
Aging leads to chronic inflammation that is linked to aging-associated conditions and diseases. Multiple immune pathways become activated during aging, posing a challenge to effectively reduce aging-associated inflammation. SIRT2, an NAD-dependent deacetylase, suppresses several immune pathways that become activated during aging and may represent an attractive target to broadly dampen aging-associated inflammation. Here, we show that SIRT2 deficiency leads to increased inflammation governed by multiple immune pathways and tissue function decline at an old age, while NAD boosting with 78c suppresses aging-associated inflammation and improves tissue function. These findings highlight SIRT2 as a master regulator of aging-associated inflammation and support NAD boosting as an effective strategy to counteract aging-associated inflammation and tissue function decline.
衰老会引发慢性炎症,而这种炎症与衰老相关的状况和疾病有关。在衰老过程中,多种免疫途径会被激活,这对有效减轻与衰老相关的炎症构成了挑战。SIRT2是一种依赖烟酰胺腺嘌呤二核苷酸(NAD)的去乙酰化酶,它能抑制在衰老过程中被激活的多种免疫途径,可能是广泛减轻与衰老相关炎症的一个有吸引力的靶点。在此,我们表明,SIRT2缺乏会导致老年时由多种免疫途径控制的炎症增加以及组织功能衰退,而用78c增强NAD可抑制与衰老相关的炎症并改善组织功能。这些发现突出了SIRT2作为与衰老相关炎症的主要调节因子,并支持增强NAD作为对抗与衰老相关炎症和组织功能衰退的有效策略。