PRMT6 inhibitors promote fracture healing by modulating osteoclast glucose metabolism.

ABSTRACT:

Introduction

Impaired fracture healing remains a significant clinical challenge due to the complexity of the healing process. Osteoclasts, derived from monocytes, are pivotal in bone tissue reconstruction, yet no effective clinical tools exist to promote fracture healing by modulating osteoclast activity.

Methods

We investigated the role of Protein Arginine Methyltransferase 6 (PRMT6) in fracture healing, focusing on its regulation of osteoclast glucose metabolism. PRMT6 deficiency and pharmacological inhibition were employed to assess its functional impact.

Results

PRMT6 was found to promote osteoclastogenesis and activate glycolysis. Both genetic deficiency and pharmacological inhibition of PRMT6 suppressed osteoclast formation and glycolytic activity. Further, PRMT

SUBMITTER: Wu N 

PROVIDER: S-EPMC12488595 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature