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Lysosomal destabilization: A missing link between pathological calcification and osteoarthritis.

Tao Ye1, Chenyu Wang1, Jianfei Yan2

  • 1State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration & National Clinical Research Center for Oral Diseases & Shaanxi Key Laboratory of Stomatology, Department of Prosthodontics, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, 710032, PR China.

Bioactive Materials
|January 4, 2024
PubMed
Summary

Hydroxyapatite in osteoarthritis cartilage causes chondrocyte cell death. Inhibiting lysosomal membrane permeabilization and cathepsin B prevents this cell death, offering a new therapeutic strategy for osteoarthritis.

Keywords:
Chondrocyte pyroptosisHydroxyapatiteLysosomal destabilizationOsteoarthritisPathological calcification

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Rheumatology

Background:

  • Hydroxyapatite deposition in cartilage is a key feature of osteoarthritis (OA), correlating with disease severity.
  • Current strategies for preventing hydroxyapatite deposition in OA cartilage are lacking.
  • The precise role of hydroxyapatite in OA pathogenesis remains debated.

Purpose of the Study:

  • To elucidate the pathogenic mechanism of intra-cartilaginous hydroxyapatite in osteoarthritis.
  • To develop strategies to counteract the detrimental effects of hydroxyapatite deposition in OA.

Main Methods:

  • Utilized in vitro and in vivo models of osteoarthritis.
  • Investigated the uptake and processing of hydroxyapatite crystallites by chondrocytes.
  • Assessed the role of lysosomal membrane permeabilization (LMP) and cathepsin B (CTSB) release.
  • Examined the activation of NLRP3 inflammasomes and subsequent chondrocyte pyroptosis.

Main Results:

  • Hydroxyapatite crystallites are phagocytized by chondrocytes and processed within lysosomes.
  • This processing leads to lysosomal membrane permeabilization (LMP) and cathepsin B (CTSB) release into the cytosol.
  • Cytosolic CTSB activates NLRP3 inflammasomes, triggering chondrocyte pyroptosis.
  • Inhibition of LMP and CTSB in vivo effectively managed osteoarthritis progression.

Conclusions:

  • Hydroxyapatite-induced lysosomal destabilization and cathepsin B release drive chondrocyte pyroptosis in osteoarthritis.
  • Targeting lysosomal membrane permeabilization and cathepsin B presents a viable therapeutic approach for osteoarthritis.
  • Alleviating lysosomal destabilization offers a conceptual solution for preventing osteoarthritis progression.