What question did this study set out to answer?

The research aims to investigate how aging affects progenitor B cell populations and subsequent osteoclast formation.

February 13, 2026Open Access

Aging-induced decrease in progenitor B cells enhances the osteoclastogenesis of bone marrow macrophages via ROS-activated Fos/CCL3 signaling pathway

RSRuiqing SunStomatology Hospital LLLan LuoFujian Medical University YCYuehua ChenBGI Group (China)

Key Points

The research aims to investigate how aging affects progenitor B cell populations and subsequent osteoclast formation.
Assessed ROS levels in the bone marrow microenvironment.
Measured progenitor B cell populations and immune-senescence markers.
Analyzed signaling pathways, particularly Fos/Jun and CCL3.
Evaluated the role of CCR1 antagonist on osteoclastogenesis.
Elevated ROS levels correlated with reduced progenitor B cell populations.
Fos/Jun pathway activation led to CCL3 overexpression.
Increased CCL3 promoted osteoclastogenesis in macrophages.
CCR1 antagonist reduced pro-inflammatory osteoclast formation.

Abstract

Our findings suggest that the elevation of ROS levels within bone marrow microenvironment accelerates immune-senescence of B lymphocytes, characterized by a significant reduction in progenitor B-cell populations, which subsequently activates the Fos/Jun-mediated stress signaling pathway. The cascade ultimately results in the overexpression of CCL3, further promoting osteoclastogenesis of macrophage through CCL3-CCR1 axis. CCR1 antagonist could alleviate pro-inflammatory osteoclast formation, revealing a potential therapeutic target for senile osteoporosis.

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Cite This Study

Sun et al. (Tue,) studied this question.

synapsesocial.com/papers/698ebf1d85a1ff6a93016432 https://doi.org/https://doi.org/10.1186/s12979-026-00561-z

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