Age-associated decline of Lamtor5 drives immunosenescence and systemic aging via cGAS-mediated paracrine inflammation.
It is demonstrated that Lamtor5 ablating macrophages displayed senescent signatures, metabolic defects, aging-related transcriptomic and epigenetic features, nicely concurring with macrophages from naturally aging mice, opening a new avenue for developing macrophage-based therapeutics to improve healthy aging.