Immune-mediated bone loss: A Mendelian randomization and NHANES-based study of viral infections and osteoporosis.

Introduction: Osteoporosis is a major risk factor for fractures, yet the contribution of immune responses to its pathogenesis remains poorly understood. This study investigates whether common viral infections, including Epstein-Barr virus (EBV), human herpesvirus 6 (HHV-6), and varicella-zoster virus (VZV), contribute to osteoporosis through immune-mediated pathways.

Methods: We performed two-sample Mendelian randomization (MR) using genome-wide association study (GWAS) summary data and complemented this with observational analyses from the NHANES 2003-2004 cycle.

End Plate Chondrocyte-Derived Exosomal miR-133a-3p Alleviates Intervertebral Disc Degeneration by Targeting the NF-κB Signaling Pathway through the miR-133a-3p/MAML1 Axis.

Chondrocyte-derived exosomes have shown efficacy in differentiating osteoarthritis-affected cartilage. Intervertebral disc degeneration (IVDD) and osteoarthritis often affect facet joints of the spine and show common epidemiological and pathophysiological characteristics. However, the potential of chondrocyte-derived exosomes for treating IVDD remains unclear.

Endplate chondrocyte-derived exosomal miR-128-3p mitigates intervertebral disc degeneration by targeting TRAF6 via the miR-128-3p/TRAF6 axis to suppress pyroptosis.

Intervertebral disc degeneration (IVDD) is a leading cause of chronic back pain and significantly impacts quality of life. The pathogenesis of IVDD is largely driven by inflammation, pyroptosis, and extracellular matrix (ECM) degradation, which current therapies fail to adequately address. In this study, we explore the therapeutic potential of exosomes derived from endplate chondrocytes (EPCs), with a particular focus on the microRNA miR-128-3p.