Nature communications · 2026
CD38-activated macrophages drive age-related placental senescence by depleting NAD+ in decidual stromal cells.
СтатьяНазвание и аннотация: Перевод в очереди
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Hua Lun, Yang Xiaohan, Gao Dengfeng, Yang Xintong, Jin Xianyang, Ma Lulu, Liu Wenting, Li Jing, Shen Zhaoli, Liu Luting, Wu Yanni, Yang Yi, Zhu Chunli, Li Litong, Jiang Xuemei, Han Xingfa, Jin Chao, Liu Guangmang, Feng Bin, Che Lianqiang, Xu Shengyu, Lin Yan, Fang Zhengfeng, Jin Long, Luo Ting, Zhuo Yong, Li Mingzhou, Wu De
Аннотация
As delayed childbearing becomes increasingly common, elucidating the mechanisms of age-related placental senescence is critical for the development of effective therapeutic strategies. Here, we integrate metabolomics, single-cell RNA sequencing, and spatial transcriptomics to uncover conserved features of aged placentas in humans, mice, and pigs, namely, increased macrophage CD38 expression and NAD⁺ deficiency. Through pharmacological and genetic approaches, we demonstrate that macrophage CD38 depletes NAD⁺ in decidual stromal cells, thereby promoting placental senescence. Mechanistically, early-onset inflammation and senescence-associated secretory phenotype activity drive CD38 expression in macrophages via the IRF5 pathway. Importantly, treatment with NAD⁺ precursors or CD38 inhibitors attenuates age-related placental senescence, rescues intrauterine growth restriction, and improves long-term metabolic outcomes in offspring. These findings reveal a critical role for macrophage-driven metabolic dysregulation in reproductive aging and establish CD38 as a potential therapeutic target for age-associated pregnancy complications.