Reducing functionally defective old HSCs alleviates aging-related phenotypes in old recipient mice
Abstract
Aging is a process accompanied by functional decline in tissues and organs with great social and medical consequences. Developing effective anti-aging strategies is of great significance. In this study, we demonstrated that transplantation of young hematopoietic stem cells (HSCs) into old mice can mitigate aging phenotypes, underscoring the crucial role of HSCs in the aging process. Through comprehensive molecular and functional analyses, we identified a subset of HSCs in aged mice that exhibit "younger" molecular profiles and functions, marked by low levels of CD150 expression. Mechanistically, CD150low HSCs from old mice can effectively differentiate into downstream lineage cells but not their CD150high counterparts. Notably, transplantation of old CD150low HSCs attenuates aging phenotypes and prolongs lifespan of elderly mice compared to those transplanted with unselected or CD150high HSCs. Importantly, reducing the dysfunctional CD150high HSCs can alleviate aging phenotypes in old recipient mice. Thus, our study demonstrates the presence of "younger" HSCs in old mice, and aging-associated functional decline can be mitigated by reducing dysfunctional HSCs.
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Research summary
The paper addresses the functional decline of hematopoietic stem cells (HSCs) in aging and presents a potential strategy for mitigating aging-related phenotypes through the transplantation of "younger" HSCs. This focus on the underlying mechanisms of aging and the potential to alleviate its effects aligns with longevity research. However, while the findings are solid and contribute to the understanding of HSCs in aging, they do not represent a major breakthrough or transformative implications for the field, thus warranting a moderate impact score.
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