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RESEARCH PAPER / 2026-02-11

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

Ruiqing Sun, Lan Luo, Yang Chen, Liangjie Sun, Yuhao Huo, Chong Ding, Yixiang Wang

Department of Pediatric Dentistry, Peking University School and Hospital of Stomatology & National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices& Beijing Key Laboratory of Digital Stomatology & NHC Key Laboratory of Digital Stomatology & NMPA Key Laboratory for Dental Materials, No.22, Zhongguancun South Avenue, Haidian District, Beijing, 100081, P.R. China.Department of Pediatric Dentistry, Peking University School and Hospital of Stomatology & National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices& Beijing Key Laboratory of Digital Stomatology & NHC Key Laboratory of Digital Stomatology & NMPA Key Laboratory for Dental Materials, No.22, Zhongguancun South Avenue, Haidian District, Beijing, 100081, P.R. China. · pubmed

Abstract

Senile osteoporosis (SOP) is becoming a critical public health burden particularly in aging societies due to escalating fracture susceptibility among elderly populations. Despite advances in SOP research, the mechanistic role of immune cell alterations in senile osteoporosis remains unclear.

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

The paper claims that aging-induced decrease in progenitor B cells enhances osteoclastogenesis in bone marrow macrophages through a specific signaling pathway. This research addresses the mechanistic role of immune cell alterations in senile osteoporosis, which is a significant age-related disease, thereby contributing to our understanding of aging processes.

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