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pink, pubmed, cartilage, article, mitochondrial, chondrocytes, pkm, mitophagy, google, scholar, fig, mice, sirt, cas, analysis, osteoarthritis, cell, cells, protein, central, glycolysis, overexpression, figs, degeneration, metabolic, mitochondria, nuclear, role, subsequently, axis, phosphorylation, deletion, bone, knockout, autophagy, cecm, cellular, significant, homeostasis, vivo, levels, minutes, function, nature, increased, staining, immunofluorescence, energy, ser, translocation,

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nature portfolio privacy policy slc25a5/ant2-pink1-prkn-mediated mitophagy specialized software tools platelet-derived growth factor-bb advertising high-resolution micro-computed tomography sequencing service pink1-pkm2-β-catenin signaling axis nature 480 nature 622 nature pink1-prkn axis-related proteins ethanol solutions mimics research software fundc1/pfkp-mediated mitophagy induced lipus-mediated anti-inflammatory effect intra-articular injection crispr-cas9-induced pink1 deletion reprints assessing high-intensity signals protein-coupled receptor class il-1β-induced oa microenvironment generate sirt3−/−pink1−/− double-knockout induces ubiquitin-dependent mitophagy hypoxia-inducible factor 1α downstream prkn-p62-lc3b cascade hif-1α-bnip3 axis sirt3-pink1 double-knockout mice subsequent research aav-pink1 injection upregulated double-knockout mice exhibited triple-negative breast cancer prkn-p62-lc3b pathway cascade pink1-ubiquitin-mediated mitophagy μ-ct imaging analyses final rate-limiting kinase glycolysis-related metabolic switch human recombinant il-1β sqstm1-dependent autophagic degradation sirt3-mediated deacetylation modification treated il-1β-impaired chondrocytes tgf-β/tak1 signaling pink1-prkn axis transitioned pink1-mediated phosphorylation modification spinal cord injury age-matched group consisted balanced c-ecm metabolism potential deacetylation-mediated relationship ultra-sensitive enhanced chemiluminescent

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         headline:SIRT3-PINK1-PKM2 axis prevents osteoarthritis via mitochondrial renewal and metabolic switch
         description:Maintaining mitochondrial homeostasis is critical for preserving chondrocyte physiological conditions and increasing resistance against osteoarthritis (OA). However, the underlying mechanisms governing mitochondrial self-renewal and energy production remain elusive. In this study, we demonstrated mitochondrial damage and aberrant mitophagy in OA chondrocytes. Genetically overexpressing PTEN-induced putative kinase 1 (PINK1) protects against cartilage degeneration by removing defective mitochondria. PINK1 knockout aggravated cartilage damage due to impaired mitophagy. SIRT3 directly deacetylated PINK1 to promote mitophagy and cartilage anabolism. Specifically, PINK1 phosphorylated PKM2 at the Ser127 site, preserving its active tetrameric form. This inhibited nuclear translocation and the interaction with β-catenin, resulting in a metabolic shift and increased energy production. Finally, a double-knockout mouse model demonstrated the role of the SIRT3-PINK1-PKM2 axis in safeguarding the structural integrity of articular joints and improving motor functions. Overall, this study provides a novel insight into the regulation of mitochondrial renewal and metabolic switches in OA.
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      description:Maintaining mitochondrial homeostasis is critical for preserving chondrocyte physiological conditions and increasing resistance against osteoarthritis (OA). However, the underlying mechanisms governing mitochondrial self-renewal and energy production remain elusive. In this study, we demonstrated mitochondrial damage and aberrant mitophagy in OA chondrocytes. Genetically overexpressing PTEN-induced putative kinase 1 (PINK1) protects against cartilage degeneration by removing defective mitochondria. PINK1 knockout aggravated cartilage damage due to impaired mitophagy. SIRT3 directly deacetylated PINK1 to promote mitophagy and cartilage anabolism. Specifically, PINK1 phosphorylated PKM2 at the Ser127 site, preserving its active tetrameric form. This inhibited nuclear translocation and the interaction with β-catenin, resulting in a metabolic shift and increased energy production. Finally, a double-knockout mouse model demonstrated the role of the SIRT3-PINK1-PKM2 axis in safeguarding the structural integrity of articular joints and improving motor functions. Overall, this study provides a novel insight into the regulation of mitochondrial renewal and metabolic switches in OA.
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            address:
               name:Orthopaedic Institute, Medical College, Soochow University, Suzhou, China
               type:PostalAddress
            type:Organization
      name:Xiaowei Xia
      affiliation:
            name:Soochow University
            address:
               name:Department of Orthopaedics, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, China
               type:PostalAddress
            type:Organization
            name:Soochow University
            address:
               name:Orthopaedic Institute, Medical College, Soochow University, Suzhou, China
               type:PostalAddress
            type:Organization
      name:Chenqi Yu
      affiliation:
            name:Soochow University
            address:
               name:Department of Orthopaedics, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, China
               type:PostalAddress
            type:Organization
            name:Soochow University
            address:
               name:Orthopaedic Institute, Medical College, Soochow University, Suzhou, China
               type:PostalAddress
            type:Organization
      name:Jianfeng Yu
      affiliation:
            name:Soochow University
            address:
               name:Department of Orthopaedics, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, China
               type:PostalAddress
            type:Organization
            name:Soochow University
            address:
               name:Orthopaedic Institute, Medical College, Soochow University, Suzhou, China
               type:PostalAddress
            type:Organization
      name:Huilin Yang
      affiliation:
            name:Soochow University
            address:
               name:Department of Orthopaedics, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, China
               type:PostalAddress
            type:Organization
            name:Soochow University
            address:
               name:Orthopaedic Institute, Medical College, Soochow University, Suzhou, China
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Yijian Zhang
      affiliation:
            name:Soochow University
            address:
               name:Department of Orthopaedics, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, China
               type:PostalAddress
            type:Organization
            name:Soochow University
            address:
               name:Orthopaedic Institute, Medical College, Soochow University, Suzhou, China
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Xuesong Zhu
      affiliation:
            name:Soochow University
            address:
               name:Department of Orthopaedics, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, China
               type:PostalAddress
            type:Organization
            name:Soochow University
            address:
               name:Orthopaedic Institute, Medical College, Soochow University, Suzhou, China
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Orthopaedics, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, China
      name:Orthopaedic Institute, Medical College, Soochow University, Suzhou, China
      name:Department of Orthopaedics, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, China
      name:Orthopaedic Institute, Medical College, Soochow University, Suzhou, China
      name:Department of Orthopaedics, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, China
      name:Orthopaedic Institute, Medical College, Soochow University, Suzhou, China
      name:Department of Orthopaedics, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, China
      name:Orthopaedic Institute, Medical College, Soochow University, Suzhou, China
      name:Department of Orthopaedics, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, China
      name:Orthopaedic Institute, Medical College, Soochow University, Suzhou, China
      name:Department of Orthopaedics, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, China
      name:Orthopaedic Institute, Medical College, Soochow University, Suzhou, China
      name:Department of Orthopaedics, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, China
      name:Orthopaedic Institute, Medical College, Soochow University, Suzhou, China
      name:Department of Orthopaedics, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, China
      name:Orthopaedic Institute, Medical College, Soochow University, Suzhou, China
      name:Department of Orthopaedics, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, China
      name:Orthopaedic Institute, Medical College, Soochow University, Suzhou, China
      name:Department of Orthopaedics, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, China
      name:Orthopaedic Institute, Medical College, Soochow University, Suzhou, China

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