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Cell Reports Medicine

Cell Reports Medicine

IF: 11.7
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Specific macrophage RhoA targeting CRISPR-Cas9 for mitigating osteoclastogenesis-induced joint damage in inflammatory arthritis

Published:15 April 2025 DOI: 10.1016/j.xcrm.2025.102046 PMID: 40239628
Jianhai Chen,?Jianwei Tan,?Nannan Wang,?Hui Li,?Wenxiang Cheng,?Jian Li,?Benguo Wang,?Adam C Sedgwick,?Zhitong Chen,?Guojun Chen,?Peng Zhang,?Wei Zheng,?Chengbo Liu,?Jingqin Chen

Abstract

Rheumatoid arthritis (RA) is the most prevalent inflammatory arthritis with unknown etiology, characterized by synovial inflammation and articular bone erosion. Studies have highlighted that inhibiting macrophage-induced osteoclastogenesis holds promise in mitigating bone destruction. However, specifically halting this pathological cascade remains a challenge for the management of RA. Here, initially, we identify that Ras homolog gene family member A (RhoA) is a pivotal target in inducing osteoclastogenesis of macrophages. Subsequently, we develop a strategy termed specific macrophages RhoA targeting (SMART), in which phosphatidylserine (PS)-enriched macrophage membranes are engineered to deliver macrophage-specific promoter-containing CRISPR-Cas9 plasmids (SMART-Cas9), enabling targeted editing of RhoA in RA joint macrophages. Multiscale imaging techniques confirm the highly specific targeted effect of SMART-Cas9 on the macrophages of inflamed joints. SMART-Cas9 successfully reduces osteoclastogenesis by macrophages, thus mitigating bone erosion by modulating cytoskeletal dynamics and immune balance in inflammatory arthritis, representing a therapeutic avenue for RA and other inflammatory bone diseases.

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