AI Article Synopsis

  • Mitochondrial dysfunction leads to increased production of reactive oxygen species (ROS), which is linked to various degenerative diseases like osteoarthritis.
  • Researchers developed a new treatment called "Mitocelle," a nanozyme made from biocompatible materials that inhibits the NOX4-p22phox interaction, which contributes to mitochondrial dysfunction.
  • In tests on a mouse model of osteoarthritis, Mitocelle demonstrated effective uptake into cartilage, long-term stability, and the ability to reduce joint damage, suggesting it could be a promising therapeutic option for related diseases.

Article Abstract

Mitochondrial dysfunction increases ROS production and is closely related to many degenerative cellular organelle diseases. The NOX4-p22phox axis is a major contributor to ROS production and its dysregulation is expected to disrupt mitochondrial function. However, the field lacks a competitive inhibitor of the NOX4-p22phox interaction. Here, we created a povidone micelle-based Prussian blue nanozyme that we named "Mitocelle" to target the NOX4-p22phox axis, and characterized its impact on the major degenerative cellular organelle disease, osteoarthritis (OA). Mitocelle is composed of FDA-approved and biocompatible materials, has a regular spherical shape, and is approximately 88 nm in diameter. Mitocelle competitively inhibits the NOX4-p22phox interaction, and its uptake by chondrocytes can protect against mitochondrial malfunction. Upon intra-articular injection to an OA mouse model, Mitocelle shows long-term stability, effective uptake into the cartilage matrix, and the ability to attenuate joint degradation. Collectively, our findings suggest that Mitocelle, which functions as a competitive inhibitor of NOX4-p22phox, may be suitable for translational research as a therapeutic for OA and cellular organelle diseases related to dysfunctional mitochondria.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11467566PMC
http://dx.doi.org/10.1016/j.bioactmat.2024.09.021DOI Listing

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