HECTD1‐Mediated Ubiquitination and Degradation of Rubicon Regulates Autophagy and Osteoarthritis Pathogenesis
Authors' conclusion
HECTD1 plays a crucial role in the pathogenesis of OA, in that HECTD1 regulates chondrocyte autophagy by ubiquitinating and targeting Rubicon for proteasomal degradation.
Study context
- Population
- Healthy human cartilage and human osteoarthritis (OA) cartilage; surgery- and aging-induced OA mouse models
- Comparison
- Human OA cartilage vs healthy cartilage; HECTD1 overexpression or conditional Hectd1 depletion in mouse OA models
Methodological detailsRNA sequencing of human cartilage, surgery- and aging-induced OA mouse models, conditional Hectd1 depletion in cartilage
- RNA sequencing of human cartilage
- Surgery- and aging-induced OA mouse models
- Conditional Hectd1 depletion in cartilage
Main finding
As reported in the abstract
- HECTD1 significantly down-regulated in human OA cartilage vs healthy cartilage
- HECTD1 overexpression in mouse joints alleviated OA pathogenesis
- Conditional Hectd1 depletion in cartilage aggravated surgery- and aging-induced OA
- HECTD1 bound Rubicon and ubiquitinated it at lysine residue 534, targeting it for proteasomal degradation
- HECTD1-mediated Rubicon degradation regulated chondrocyte autophagy, mitigating stress-induced chondrocyte death and OA progression
Original publication
HECTD1‐Mediated Ubiquitination and Degradation of Rubicon Regulates Autophagy and Osteoarthritis Pathogenesis. Arthritis Rheumatol. Published 25 January 2023. doi:10.
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