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      Effect of mitophagy in the formation of osteomorphs derived from osteoclasts

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          Summary

          Osteoclasts are specialized multinucleated giant cells with unique bone-destroying capacities. A recent study revealed that osteoclasts undergo an alternative cell fate by dividing into daughter cells called osteomorphs. To date, no studies have focused on the mechanisms of osteoclast fission. In this study, we analyzed the alternative cell fate process in vitro and, herein, reported the high expression of mitophagy-related proteins during osteoclast fission. Mitophagy was further confirmed by the colocalization of mitochondria with lysosomes, as observed in fluorescence images and transmission electron microscopy. We investigated the role played by mitophagy in osteoclast fission via drug stimulation experiments. The results showed that mitophagy promoted osteoclast division, and inhibition of mitophagy induced osteoclast apoptosis. In summary, this study reveals the role played by mitophagy as the decisive link in osteoclasts’ fate, providing a new therapeutic target and perspective for the clinical treatment of osteoclast-related diseases.

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          Highlights

          • •

            Mitophagy is involved in the osteoclast-osteomorph transformation

          • •

            Enhancing mitophagy promotes osteomorph formation

          • •

            Mitophagy determines whether osteoclasts undergo apoptosis or fission

          Abstract

          Molecular interaction; Specialized functions of cells; Functional aspects of cell biology

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          Most cited references73

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          Osteoporosis: now and the future.

          Tilman Rachner, Sundeep Khosla, Lorenz Hofbauer (2011)
          Osteoporosis is a common disease characterised by a systemic impairment of bone mass and microarchitecture that results in fragility fractures. With an ageing population, the medical and socioeconomic effect of osteoporosis, particularly postmenopausal osteoporosis, will increase further. A detailed knowledge of bone biology with molecular insights into the communication between bone-forming osteoblasts and bone-resorbing osteoclasts and the orchestrating signalling network has led to the identification of novel therapeutic targets. Novel treatment strategies have been developed that aim to inhibit excessive bone resorption and increase bone formation. The most promising novel treatments include: denosumab, a monoclonal antibody for receptor activator of NF-κB ligand, a key osteoclast cytokine; odanacatib, a specific inhibitor of the osteoclast protease cathepsin K; and antibodies against the proteins sclerostin and dickkopf-1, two endogenous inhibitors of bone formation. This overview discusses these novel therapies and explains their underlying physiology. Copyright © 2011 Elsevier Ltd. All rights reserved.
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            Mitophagy inhibits amyloid-β and tau pathology and reverses cognitive deficits in models of Alzheimer’s disease

            Evandro F Fang, Yujun Hou, Konstantinos Palikaras … (2019)
            Accumulation of damaged mitochondria is a hallmark of aging and age-related neurodegeneration, including Alzheimer's disease (AD). The molecular mechanisms of impaired mitochondrial homeostasis in AD are being investigated. Here we provide evidence that mitophagy is impaired in the hippocampus of AD patients, in induced pluripotent stem cell-derived human AD neurons, and in animal AD models. In both amyloid-β (Aβ) and tau Caenorhabditis elegans models of AD, mitophagy stimulation (through NAD+ supplementation, urolithin A, and actinonin) reverses memory impairment through PINK-1 (PTEN-induced kinase-1)-, PDR-1 (Parkinson's disease-related-1; parkin)-, or DCT-1 (DAF-16/FOXO-controlled germline-tumor affecting-1)-dependent pathways. Mitophagy diminishes insoluble Aβ1-42 and Aβ1-40 and prevents cognitive impairment in an APP/PS1 mouse model through microglial phagocytosis of extracellular Aβ plaques and suppression of neuroinflammation. Mitophagy enhancement abolishes AD-related tau hyperphosphorylation in human neuronal cells and reverses memory impairment in transgenic tau nematodes and mice. Our findings suggest that impaired removal of defective mitochondria is a pivotal event in AD pathogenesis and that mitophagy represents a potential therapeutic intervention.
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              Mitochondrial Dynamics and Its Involvement in Disease

              David Chan (2020)
              The dynamic properties of mitochondria—including their fusion, fission, and degradation—are critical for their optimal function in energy generation. The interplay of fusion and fission confers widespread benefits on mitochondria, including efficient transport, increased homogenization of the mitochondrial population, and efficient oxidative phosphorylation. These benefits arise through control of morphology, content exchange, equitable inheritance of mitochondria, maintenance of high-quality mitochondrial DNA, and segregation of damaged mitochondria for degradation. The key components of the machinery mediating mitochondrial fusion and fission belong to the dynamin family of GTPases that utilize GTP hydrolysis to drive mechanical work on biological membranes. Defects in this machinery cause a range of diseases that especially affect the nervous system. In addition, several common diseases, including neurodegenerative diseases and cancer, strongly affect mitochondrial dynamics.
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                Author and article information

                Contributors
                Ying Wang
                Guoli Yang
                Journal
                Journal ID (nlm-ta): iScience
                Journal ID (iso-abbrev): iScience
                Title: iScience
                Publisher: Elsevier
                ISSN (Electronic): 2589-0042
                Publication date PMC-release: 18 April 2023
                Publication date Collection: 19 May 2023
                Publication date (Electronic): 18 April 2023
                Volume: 26
                Issue: 5
                Electronic Location Identifier: 106682
                Affiliations
                [1 ]Stomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center for Oral Diseases, Key Laboratory of Oral Biomedical Research of Zhejiang Province, Cancer Center of Zhejiang University, Hangzhou, Zhejiang 310006, China
                [2 ]Department of Implantology, The Affiliated Stomatology Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310006, China
                [3 ]Department of Endodontics, The Affiliated Stomatology Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310006, China
                Author notes
                [∗ ]Corresponding author 7314032@ 123456zju.edu.cn
                [∗∗ ]Corresponding author guo_li1214@ 123456zju.edu.cn
                [4]

                These authors contributed equally

                [5]

                Lead contact

                Article
                Publisher Item ID: S2589-0042(23)00759-9 Publisher ID: 106682
                DOI: 10.1016/j.isci.2023.106682
                PMC ID: 10214740
                PubMed ID: 37250312
                SO-VID: a69dd710-805c-4cb5-b980-96ea88816617
                Copyright © © 2023 The Authors
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 29 April 2022
                Date revision received : 27 January 2023
                Date accepted : 12 April 2023
                Categories
                Subject: Article

                Keywords: molecular interaction,specialized functions of cells,functional aspects of cell biology
                Data availability:
                Keywords: molecular interaction, specialized functions of cells, functional aspects of cell biology

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