ArticleClinical and translational medicine2024
Genetically inspired organoids prevent joint degeneration and alleviate chondrocyte senescence via Col11a1-HIF1α-mediated glycolysis-OXPHOS metabolism shift.
Article in Clinical and translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 14 citations in OpenAlex.
- SETD1A Regulates Glycolysis and Senescence of Nucleus Pulposus Cells via H3K4me3-HELZ2/PPARα-HIF1α Axis to Drive Intervertebral Disc Degeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cellular mechanometabolism: stimuli and implications.EMBO reports · 2026Review
- Construction of biomimetic gradient-structured cartilage organoids and mechanistic study of their application for cartilage rejuvenation.Bioactive materials · 2026Article
- Transcriptomics in the Study of Bone and Cartilage.Current osteoporosis reports · 2026Review
- seneR: An R package for comprehensive senescence assessment and its application in type 2 diabetes and osteoarthritis.Computational and structural biotechnology journal · 2026Article
- Immunometabolic dysregulation in autoimmune rheumatic diseases: the central role of glycolytic reprogramming in pathogenesis and traditional Chinese medicine therapy.Frontiers in immunology · 2026Review
- Review
- Innovative strategies for bone organoid: Synergistic application and exploration of advanced technologies.Journal of orthopaedic translation · 2025Review
- Genetics of morphological hip abnormalities and their implications for osteoarthritis: a scoping review.Journal of hip preservation surgery · 2025Review
- Bone organoid construction and evolution.Journal of orthopaedic translation · 2025Review
- Selection of experimental animals and modeling methods in developmental dysplasia of the hip research.EFORT open reviews · 2025Review
- Intelligent Manufacturing for Osteoarthritis Organoids.Cell proliferation · 2025Review
- SIRT3-PINK1-PKM2 axis prevents osteoarthritis via mitochondrial renewal and metabolic switch.Bone research · 2025Article
- Genetically inspired organoids prevent joint degeneration and alleviate chondrocyte senescence via Col11a1-HIF1α-mediated glycolysis-OXPHOS metabolism shift.Clinical and translational medicine · 2024Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
introductionDevelopmental dysplasia of hip (DDH) is a hip joint disorder leading to subsequent osteoarthritis. Previous studies suggested collagen XI alpha 1 (COL11A1) as a potential gene in hip dysplasia and chondrocyte degeneration. However, no genetic association has reported COL11A1-related cellular therapy as treatment of DDH and joint degeneration. METHODS AND
resultsWe report identified genetic association between COL11A1 locus and DDH with genome-wide association study (GWAS). Further exome sequencing for familial DDH patients was conducted in different populations to identify potential pathogenic Col11A1 variants for familiar DDH. Further studies demonstrated involvement of COL11A1 expression was down-regulated in femoral head cartilage of DDH patients and Col11a1-KO mice with induced DDH. Col11a1-KO mice demonstrated aggravated joint degeneration and severe OA phenotype. To explore the underlying mechanism of Col11a1 in cartilage and DDH development, we generated scRNA-seq profiles for DDH and Col11a1-KO cartilage, demonstrating disrupted chondrocyte homeostasis and cellular senescence caused by Col11a1-HIF1α-mediated glycolysis-OXPHOS shift in chondrocytes. Genetically and biologically inspired, we further fabricated an intra-articular injection therapy to preventing cartilage degeneration by generating a Col11a1-over-expressed (OE) SMSC mini-organoids. Col11a1-OE organoids demonstrated superior chondrogenesis and ameliorated cartilage degeneration in DDH mice via regulating cellular senescence by up-regulated Col11a1/HIF1α-mediated glycolysis in chondrocytes.
conclusionWe reported association between COL11A1 loci and DDH with GWAS and exome sequencing. Further studies demonstrated involvement of COL11A1 in DDH patients and Col11a1-KO mice. ScRNA-seq for DDH and Col11a1-KO cartilage demonstrated disrupted chondrocyte homeostasis and cellular senescence caused by Col11a1-HIF1α-mediated glycolysis-OXPHOS shift in chondrocytes. Genetically and biologically inspired, an intra-articular injection therapy was fabricated to prevent cartilage degeneration with Col11a1-OE SMSC organoids. Col11a1-OE organoids ameliorated cartilage degeneration in DDH mice via regulating cellular senescence by up-regulated Col11a1/HIF1α-mediated glycolysis in chondrocytes.
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