Mitochondrial dysfunction and therapeutic perspectives in osteoporosis

Osteoporosis (OP) is a systemic skeletal disorder characterized by reduced bone mass and structural deterioration of bone tissue, resulting in heightened vulnerability to fractures due to increased bone fragility. This condition primarily arises from an imbalance between the processes of bone resorp...

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Main Authors: Jialing Liu, Zhonghua Gao, Xiangjie Liu
Format: Article
Language:English
Published: Frontiers Media S.A. 2024-02-01
Series:Frontiers in Endocrinology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fendo.2024.1325317/full
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author Jialing Liu
Zhonghua Gao
Xiangjie Liu
author_facet Jialing Liu
Zhonghua Gao
Xiangjie Liu
author_sort Jialing Liu
collection DOAJ
description Osteoporosis (OP) is a systemic skeletal disorder characterized by reduced bone mass and structural deterioration of bone tissue, resulting in heightened vulnerability to fractures due to increased bone fragility. This condition primarily arises from an imbalance between the processes of bone resorption and formation. Mitochondrial dysfunction has been reported to potentially constitute one of the most crucial mechanisms influencing the pathogenesis of osteoporosis. In essence, mitochondria play a crucial role in maintaining the delicate equilibrium between bone formation and resorption, thereby ensuring optimal skeletal health. Nevertheless, disruption of this delicate balance can arise as a consequence of mitochondrial dysfunction. In dysfunctional mitochondria, the mitochondrial electron transport chain (ETC) becomes uncoupled, resulting in reduced ATP synthesis and increased generation of reactive oxygen species (ROS). Reinforcement of mitochondrial dysfunction is further exacerbated by the accumulation of aberrant mitochondria. In this review, we investigated and analyzed the correlation between mitochondrial dysfunction, encompassing mitochondrial DNA (mtDNA) alterations, oxidative phosphorylation (OXPHOS) impairment, mitophagy dysregulation, defects in mitochondrial biogenesis and dynamics, as well as excessive ROS accumulation, with regards to OP (Figure 1). Furthermore, we explore prospective strategies currently available for modulating mitochondria to ameliorate osteoporosis. Undoubtedly, certain therapeutic strategies still require further investigation to ensure their safety and efficacy as clinical treatments. However, from a mitochondrial perspective, the potential for establishing effective and safe therapeutic approaches for osteoporosis appears promising.
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spelling doaj.art-a6386690e2f54a5396a7b26ee7a6a35e2024-02-02T09:26:46ZengFrontiers Media S.A.Frontiers in Endocrinology1664-23922024-02-011510.3389/fendo.2024.13253171325317Mitochondrial dysfunction and therapeutic perspectives in osteoporosisJialing Liu0Zhonghua Gao1Xiangjie Liu2Department of Geriatrics, Liyuan Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaSchool of Medicine, Ezhou Vocational University, Ezhou, ChinaDepartment of Geriatrics, Liyuan Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaOsteoporosis (OP) is a systemic skeletal disorder characterized by reduced bone mass and structural deterioration of bone tissue, resulting in heightened vulnerability to fractures due to increased bone fragility. This condition primarily arises from an imbalance between the processes of bone resorption and formation. Mitochondrial dysfunction has been reported to potentially constitute one of the most crucial mechanisms influencing the pathogenesis of osteoporosis. In essence, mitochondria play a crucial role in maintaining the delicate equilibrium between bone formation and resorption, thereby ensuring optimal skeletal health. Nevertheless, disruption of this delicate balance can arise as a consequence of mitochondrial dysfunction. In dysfunctional mitochondria, the mitochondrial electron transport chain (ETC) becomes uncoupled, resulting in reduced ATP synthesis and increased generation of reactive oxygen species (ROS). Reinforcement of mitochondrial dysfunction is further exacerbated by the accumulation of aberrant mitochondria. In this review, we investigated and analyzed the correlation between mitochondrial dysfunction, encompassing mitochondrial DNA (mtDNA) alterations, oxidative phosphorylation (OXPHOS) impairment, mitophagy dysregulation, defects in mitochondrial biogenesis and dynamics, as well as excessive ROS accumulation, with regards to OP (Figure 1). Furthermore, we explore prospective strategies currently available for modulating mitochondria to ameliorate osteoporosis. Undoubtedly, certain therapeutic strategies still require further investigation to ensure their safety and efficacy as clinical treatments. However, from a mitochondrial perspective, the potential for establishing effective and safe therapeutic approaches for osteoporosis appears promising.https://www.frontiersin.org/articles/10.3389/fendo.2024.1325317/fullosteoporosismitochondrial dysfunctionoxidative phosphorylationreactive oxygen speciesmitochondrial quality control
spellingShingle Jialing Liu
Zhonghua Gao
Xiangjie Liu
Mitochondrial dysfunction and therapeutic perspectives in osteoporosis
Frontiers in Endocrinology
osteoporosis
mitochondrial dysfunction
oxidative phosphorylation
reactive oxygen species
mitochondrial quality control
title Mitochondrial dysfunction and therapeutic perspectives in osteoporosis
title_full Mitochondrial dysfunction and therapeutic perspectives in osteoporosis
title_fullStr Mitochondrial dysfunction and therapeutic perspectives in osteoporosis
title_full_unstemmed Mitochondrial dysfunction and therapeutic perspectives in osteoporosis
title_short Mitochondrial dysfunction and therapeutic perspectives in osteoporosis
title_sort mitochondrial dysfunction and therapeutic perspectives in osteoporosis
topic osteoporosis
mitochondrial dysfunction
oxidative phosphorylation
reactive oxygen species
mitochondrial quality control
url https://www.frontiersin.org/articles/10.3389/fendo.2024.1325317/full
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AT xiangjieliu mitochondrialdysfunctionandtherapeuticperspectivesinosteoporosis