Palladium Nanoparticles Degrade Advanced Glycation End Products via Valosin‐Containing Protein Mediated Autophagy to Attenuate High‐Glucose/High‐Fat‐Induced Intervertebral Disc Degeneration
ABSTRACT Intervertebral disc degeneration (IVDD) is a chronic musculoskeletal disorder causing lower back pain, imposing a considerable burden on global health. Hyperglycemia resulting from diabetes mellitus induces advanced glycation end products (AGEs) accumulation in nucleus pulposus cells, leadi...
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| Published in | Exploration (Beijing, China) Vol. 5; no. 2; pp. 20230174 - n/a |
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| Main Authors | , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
China
John Wiley & Sons, Inc
01.04.2025
John Wiley and Sons Inc Wiley |
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| Online Access | Get full text |
| ISSN | 2766-8509 2766-2098 2766-2098 |
| DOI | 10.1002/EXP.20230174 |
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| Abstract | ABSTRACT
Intervertebral disc degeneration (IVDD) is a chronic musculoskeletal disorder causing lower back pain, imposing a considerable burden on global health. Hyperglycemia resulting from diabetes mellitus induces advanced glycation end products (AGEs) accumulation in nucleus pulposus cells, leading to IVDD. Mitigating AGEs accumulation is a novel promising strategy for IVDD management. In our study, palladium nanoparticles (Pd NPs) preferentially colocalized within the endoplasmic reticulum and efficiently degraded AGEs via valosin‐containing protein (VCP)‐mediated autophagy pathways. Pd NPs promoted the ATPase activity of VCPs, upregulated microtubule‐associated proteins 1A/1B light chain 3 (LC3) expression, and increased AGEs‐degrading autophagosome production. They ameliorated mitochondrial function, relieved endoplasmic reticulum stress, and counteracted the detrimental oxidative stress microenvironment in a high‐glucose/high‐fat‐induced nucleus pulposus cell degeneration model. Consequently, Pd NPs effectively rescued nucleus pulposus cell degeneration in vitro, restored disc height and partially recovered the degenerated phenotype of IVDD in vivo. We provide novel insights regarding IVDD management by targeting AGEs degradation, showing potential for clinical practice.
Illustration of Pd NP‐mediated rescue of HGHF (or advanced glycation end products [AGEs])‐induced IVD degeneration by targeting AGEs degradation. Pd NPs promote the ATPase activity of VCP and upregulate autophagosome formation to degrade AGEs. Consequently, Pd NPs alleviate the oxidative and ER stress, protect the structure and function of mitochondria, and eventually facilitate IVDD mitigation. Created with BioRender.com (Agreement No. JU26337Q4Q). |
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| AbstractList | ABSTRACT Intervertebral disc degeneration (IVDD) is a chronic musculoskeletal disorder causing lower back pain, imposing a considerable burden on global health. Hyperglycemia resulting from diabetes mellitus induces advanced glycation end products (AGEs) accumulation in nucleus pulposus cells, leading to IVDD. Mitigating AGEs accumulation is a novel promising strategy for IVDD management. In our study, palladium nanoparticles (Pd NPs) preferentially colocalized within the endoplasmic reticulum and efficiently degraded AGEs via valosin‐containing protein (VCP)‐mediated autophagy pathways. Pd NPs promoted the ATPase activity of VCPs, upregulated microtubule‐associated proteins 1A/1B light chain 3 (LC3) expression, and increased AGEs‐degrading autophagosome production. They ameliorated mitochondrial function, relieved endoplasmic reticulum stress, and counteracted the detrimental oxidative stress microenvironment in a high‐glucose/high‐fat‐induced nucleus pulposus cell degeneration model. Consequently, Pd NPs effectively rescued nucleus pulposus cell degeneration in vitro, restored disc height and partially recovered the degenerated phenotype of IVDD in vivo. We provide novel insights regarding IVDD management by targeting AGEs degradation, showing potential for clinical practice. Intervertebral disc degeneration (IVDD) is a chronic musculoskeletal disorder causing lower back pain, imposing a considerable burden on global health. Hyperglycemia resulting from diabetes mellitus induces advanced glycation end products (AGEs) accumulation in nucleus pulposus cells, leading to IVDD. Mitigating AGEs accumulation is a novel promising strategy for IVDD management. In our study, palladium nanoparticles (Pd NPs) preferentially colocalized within the endoplasmic reticulum and efficiently degraded AGEs via valosin‐containing protein (VCP)‐mediated autophagy pathways. Pd NPs promoted the ATPase activity of VCPs, upregulated microtubule‐associated proteins 1A/1B light chain 3 (LC3) expression, and increased AGEs‐degrading autophagosome production. They ameliorated mitochondrial function, relieved endoplasmic reticulum stress, and counteracted the detrimental oxidative stress microenvironment in a high‐glucose/high‐fat‐induced nucleus pulposus cell degeneration model. Consequently, Pd NPs effectively rescued nucleus pulposus cell degeneration in vitro, restored disc height and partially recovered the degenerated phenotype of IVDD in vivo. We provide novel insights regarding IVDD management by targeting AGEs degradation, showing potential for clinical practice. Intervertebral disc degeneration (IVDD) is a chronic musculoskeletal disorder causing lower back pain, imposing a considerable burden on global health. Hyperglycemia resulting from diabetes mellitus induces advanced glycation end products (AGEs) accumulation in nucleus pulposus cells, leading to IVDD. Mitigating AGEs accumulation is a novel promising strategy for IVDD management. In our study, palladium nanoparticles (Pd NPs) preferentially colocalized within the endoplasmic reticulum and efficiently degraded AGEs via valosin‐containing protein (VCP)‐mediated autophagy pathways. Pd NPs promoted the ATPase activity of VCPs, upregulated microtubule‐associated proteins 1A/1B light chain 3 (LC3) expression, and increased AGEs‐degrading autophagosome production. They ameliorated mitochondrial function, relieved endoplasmic reticulum stress, and counteracted the detrimental oxidative stress microenvironment in a high‐glucose/high‐fat‐induced nucleus pulposus cell degeneration model. Consequently, Pd NPs effectively rescued nucleus pulposus cell degeneration in vitro, restored disc height and partially recovered the degenerated phenotype of IVDD in vivo. We provide novel insights regarding IVDD management by targeting AGEs degradation, showing potential for clinical practice. Illustration of Pd NP‐mediated rescue of HGHF (or advanced glycation end products [AGEs])‐induced IVD degeneration by targeting AGEs degradation. Pd NPs promote the ATPase activity of VCP and upregulate autophagosome formation to degrade AGEs. Consequently, Pd NPs alleviate the oxidative and ER stress, protect the structure and function of mitochondria, and eventually facilitate IVDD mitigation. Created with BioRender.com (Agreement No. JU26337Q4Q). ABSTRACT Intervertebral disc degeneration (IVDD) is a chronic musculoskeletal disorder causing lower back pain, imposing a considerable burden on global health. Hyperglycemia resulting from diabetes mellitus induces advanced glycation end products (AGEs) accumulation in nucleus pulposus cells, leading to IVDD. Mitigating AGEs accumulation is a novel promising strategy for IVDD management. In our study, palladium nanoparticles (Pd NPs) preferentially colocalized within the endoplasmic reticulum and efficiently degraded AGEs via valosin‐containing protein (VCP)‐mediated autophagy pathways. Pd NPs promoted the ATPase activity of VCPs, upregulated microtubule‐associated proteins 1A/1B light chain 3 (LC3) expression, and increased AGEs‐degrading autophagosome production. They ameliorated mitochondrial function, relieved endoplasmic reticulum stress, and counteracted the detrimental oxidative stress microenvironment in a high‐glucose/high‐fat‐induced nucleus pulposus cell degeneration model. Consequently, Pd NPs effectively rescued nucleus pulposus cell degeneration in vitro, restored disc height and partially recovered the degenerated phenotype of IVDD in vivo. We provide novel insights regarding IVDD management by targeting AGEs degradation, showing potential for clinical practice. Illustration of Pd NP‐mediated rescue of HGHF (or advanced glycation end products [AGEs])‐induced IVD degeneration by targeting AGEs degradation. Pd NPs promote the ATPase activity of VCP and upregulate autophagosome formation to degrade AGEs. Consequently, Pd NPs alleviate the oxidative and ER stress, protect the structure and function of mitochondria, and eventually facilitate IVDD mitigation. Created with BioRender.com (Agreement No. JU26337Q4Q). Intervertebral disc degeneration (IVDD) is a chronic musculoskeletal disorder causing lower back pain, imposing a considerable burden on global health. Hyperglycemia resulting from diabetes mellitus induces advanced glycation end products (AGEs) accumulation in nucleus pulposus cells, leading to IVDD. Mitigating AGEs accumulation is a novel promising strategy for IVDD management. In our study, palladium nanoparticles (Pd NPs) preferentially colocalized within the endoplasmic reticulum and efficiently degraded AGEs via valosin-containing protein (VCP)-mediated autophagy pathways. Pd NPs promoted the ATPase activity of VCPs, upregulated microtubule-associated proteins 1A/1B light chain 3 (LC3) expression, and increased AGEs-degrading autophagosome production. They ameliorated mitochondrial function, relieved endoplasmic reticulum stress, and counteracted the detrimental oxidative stress microenvironment in a high-glucose/high-fat-induced nucleus pulposus cell degeneration model. Consequently, Pd NPs effectively rescued nucleus pulposus cell degeneration in vitro, restored disc height and partially recovered the degenerated phenotype of IVDD in vivo. We provide novel insights regarding IVDD management by targeting AGEs degradation, showing potential for clinical practice.Intervertebral disc degeneration (IVDD) is a chronic musculoskeletal disorder causing lower back pain, imposing a considerable burden on global health. Hyperglycemia resulting from diabetes mellitus induces advanced glycation end products (AGEs) accumulation in nucleus pulposus cells, leading to IVDD. Mitigating AGEs accumulation is a novel promising strategy for IVDD management. In our study, palladium nanoparticles (Pd NPs) preferentially colocalized within the endoplasmic reticulum and efficiently degraded AGEs via valosin-containing protein (VCP)-mediated autophagy pathways. Pd NPs promoted the ATPase activity of VCPs, upregulated microtubule-associated proteins 1A/1B light chain 3 (LC3) expression, and increased AGEs-degrading autophagosome production. They ameliorated mitochondrial function, relieved endoplasmic reticulum stress, and counteracted the detrimental oxidative stress microenvironment in a high-glucose/high-fat-induced nucleus pulposus cell degeneration model. Consequently, Pd NPs effectively rescued nucleus pulposus cell degeneration in vitro, restored disc height and partially recovered the degenerated phenotype of IVDD in vivo. We provide novel insights regarding IVDD management by targeting AGEs degradation, showing potential for clinical practice. |
| Author | Rong, Kewei Cao, Xiankun Yang, Yangzi Wang, Xin Lu, Liqiang Fu, Jingke Zhang, Kai Yang, Xiao Hao, Yongqiang Guo, Jiadong Yang, Huan Zhou, Tangjun Zhao, Jie Zhang, Pu |
| AuthorAffiliation | 4 The Second Clinical Medical College of Yunnan University of Traditional Chinese Medicine Kunming China 2 Department of Orthopedic Surgery Spine Center Changzheng Hospital Navy Medical University Shanghai China 3 Institute of Electrochemical Energy Storage Helmholtz‐Zentrum Berlin für Materialien und Energie Berlin Germany 1 Shanghai Key Laboratory of Orthopedic Implants Department of Orthopedics Ninth People's Hospital Shanghai Jiao Tong University School of Medicine Shanghai China |
| AuthorAffiliation_xml | – name: 4 The Second Clinical Medical College of Yunnan University of Traditional Chinese Medicine Kunming China – name: 2 Department of Orthopedic Surgery Spine Center Changzheng Hospital Navy Medical University Shanghai China – name: 3 Institute of Electrochemical Energy Storage Helmholtz‐Zentrum Berlin für Materialien und Energie Berlin Germany – name: 1 Shanghai Key Laboratory of Orthopedic Implants Department of Orthopedics Ninth People's Hospital Shanghai Jiao Tong University School of Medicine Shanghai China |
| Author_xml | – sequence: 1 givenname: Xiao surname: Yang fullname: Yang, Xiao organization: Shanghai Jiao Tong University School of Medicine – sequence: 2 givenname: Xiankun surname: Cao fullname: Cao, Xiankun organization: Shanghai Jiao Tong University School of Medicine – sequence: 3 givenname: Xin surname: Wang fullname: Wang, Xin organization: Shanghai Jiao Tong University School of Medicine – sequence: 4 givenname: Jiadong surname: Guo fullname: Guo, Jiadong organization: Shanghai Jiao Tong University School of Medicine – sequence: 5 givenname: Yangzi surname: Yang fullname: Yang, Yangzi organization: Navy Medical University – sequence: 6 givenname: Liqiang surname: Lu fullname: Lu, Liqiang organization: Helmholtz‐Zentrum Berlin für Materialien und Energie – sequence: 7 givenname: Pu surname: Zhang fullname: Zhang, Pu organization: Shanghai Jiao Tong University School of Medicine – sequence: 8 givenname: Huan surname: Yang fullname: Yang, Huan organization: The Second Clinical Medical College of Yunnan University of Traditional Chinese Medicine – sequence: 9 givenname: Kewei surname: Rong fullname: Rong, Kewei organization: Shanghai Jiao Tong University School of Medicine – sequence: 10 givenname: Tangjun surname: Zhou fullname: Zhou, Tangjun organization: Shanghai Jiao Tong University School of Medicine – sequence: 11 givenname: Yongqiang surname: Hao fullname: Hao, Yongqiang organization: Shanghai Jiao Tong University School of Medicine – sequence: 12 givenname: Jie surname: Zhao fullname: Zhao, Jie email: profzhaojie@126.com organization: Shanghai Jiao Tong University School of Medicine – sequence: 13 givenname: Jingke orcidid: 0000-0003-0554-9046 surname: Fu fullname: Fu, Jingke email: fujingke@sjtu.edu.cn organization: Shanghai Jiao Tong University School of Medicine – sequence: 14 givenname: Kai surname: Zhang fullname: Zhang, Kai email: orth_kai@163.com organization: Shanghai Jiao Tong University School of Medicine |
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| Copyright | 2025 The Author(s). published by Henan University and John Wiley & Sons Australia, Ltd. 2025 The Author(s). Exploration published by Henan University and John Wiley & Sons Australia, Ltd. 2025. This work is published under http://creativecommons.org/licenses/by/4.0/ (the "License"). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| Keywords | intervertebral disc degeneration palladium nanoparticles advanced glycation end products nucleus pulposus high‐glucose/high‐fat |
| Language | English |
| License | Attribution 2025 The Author(s). Exploration published by Henan University and John Wiley & Sons Australia, Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
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| Notes | This study was supported by grants from the National Natural Science Foundation of China (Nos. 82130073, 82202737, and 82302722), National Key Research and Development Program of China (No. 2022YFC2406000), Shanghai Frontiers Science Center of Degeneration and Regeneration in Skeletal System, Biomaterials and Regenerative Medicine Institute Cooperative Research Project, Shanghai Jiao Tong University School of Medicine (No. 2022LHA01), and Fundamental Research Program funding of Ninth People's Hospital affiliated to Shanghai Jiao Tong University School of Medicine (JYZZ215). Xiao Yang, Xiankun Cao, and Xin Wang contributed equally to this work. Funding statement ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Funding statement: This study was supported by grants from the National Natural Science Foundation of China (Nos. 82130073, 82202737, and 82302722), National Key Research and Development Program of China (No. 2022YFC2406000), Shanghai Frontiers Science Center of Degeneration and Regeneration in Skeletal System, Biomaterials and Regenerative Medicine Institute Cooperative Research Project, Shanghai Jiao Tong University School of Medicine (No. 2022LHA01), and Fundamental Research Program funding of Ninth People's Hospital affiliated to Shanghai Jiao Tong University School of Medicine (JYZZ215). |
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Intervertebral disc degeneration (IVDD) is a chronic musculoskeletal disorder causing lower back pain, imposing a considerable burden on global... Intervertebral disc degeneration (IVDD) is a chronic musculoskeletal disorder causing lower back pain, imposing a considerable burden on global health.... ABSTRACT Intervertebral disc degeneration (IVDD) is a chronic musculoskeletal disorder causing lower back pain, imposing a considerable burden on global... |
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| SubjectTerms | Accumulation advanced glycation end products Advanced glycosylation end products Autophagy Back pain Degeneration Degenerative disc disease Diabetes mellitus Endoplasmic reticulum Global health Glucose high‐glucose/high‐fat Hyperglycemia intervertebral disc degeneration Intervertebral discs Low back pain Microenvironments Microscopy Musculoskeletal diseases Nanoparticles Nuclei (cytology) Nucleus pulposus Oxidative stress Palladium palladium nanoparticles Phenotypes Proteins Public health |
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| Title | Palladium Nanoparticles Degrade Advanced Glycation End Products via Valosin‐Containing Protein Mediated Autophagy to Attenuate High‐Glucose/High‐Fat‐Induced Intervertebral Disc Degeneration |
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