Age-related IGF-1 decline permits a redox-sensitive transcriptional shift that directs hematopoiesis toward a CCR2
Abstract
Aging reshapes hematopoiesis toward myelopoiesis, particularly increased output of classical monocytes, contributing to immunosenescence. However, the underlying mechanisms remain unclear. Here, we identify that aging drives hematopoietic stem cells (HSCs) to progressively commit to a CCR2
The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.
Research summary
Aging-induced decline in IGF-1 triggers a redox-sensitive transcriptional shift that drives hematopoietic stem cells toward CCR2+ monocyte production. This paper is relevant because it identifies a specific upstream molecular mechanism (IGF-1/redox signaling) driving a fundamental age-related physiological change (myelopoiesis bias), offering a potential target for intervening in the root causes of immunosenescence rather than just treating downstream symptoms.
Author of this paper? Send a correction.