The role of reactive oxygen species in bone cell physiology and pathophysiology
Hydrogen peroxide (H2O2), superoxide anion radical (O2−), and other forms of reactive oxygen species (ROS) are produced by the vast majority of mammalian cells and can contribute both to cellular homeostasis and dysfunction. The NADPH oxidases (NOX) enzymes and the mitochondria electron transport ch...
| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2023-12-01
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| Series: | Bone Reports |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2352187223000128 |
| _version_ | 1797398593135443968 |
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| author | Adriana Marques-Carvalho Ha-Neui Kim Maria Almeida |
| author_facet | Adriana Marques-Carvalho Ha-Neui Kim Maria Almeida |
| author_sort | Adriana Marques-Carvalho |
| collection | DOAJ |
| description | Hydrogen peroxide (H2O2), superoxide anion radical (O2−), and other forms of reactive oxygen species (ROS) are produced by the vast majority of mammalian cells and can contribute both to cellular homeostasis and dysfunction. The NADPH oxidases (NOX) enzymes and the mitochondria electron transport chain (ETC) produce most of the cellular ROS. Multiple antioxidant systems prevent the accumulation of excessive amounts of ROS which cause damage to all cellular macromolecules. Many studies have examined the contribution of ROS to different bone cell types and to skeletal physiology and pathophysiology. Here, we discuss the role of H2O2 and O2− and their major enzymatic sources in osteoclasts and osteoblasts, the fundamentally different ways via which these cell types utilize mitochondrial derived H2O2 for differentiation and function, and the molecular mechanisms that impact and are altered by ROS in these cells. Particular emphasis is placed on evidence obtained from mouse models describing the contribution of different sources of ROS or antioxidant enzymes to bone resorption and formation. Findings from studies using pharmacological or genetically modified mouse models indicate that an increase in H2O2 and perhaps other ROS contribute to the loss of bone mass with aging and estrogen deficiency, the two most important causes of osteoporosis and increased fracture risk in humans. |
| first_indexed | 2024-03-09T01:27:48Z |
| format | Article |
| id | doaj.art-d42625e9d2854f18b16f079c4b1bd8c2 |
| institution | Directory Open Access Journal |
| issn | 2352-1872 |
| language | English |
| last_indexed | 2024-03-09T01:27:48Z |
| publishDate | 2023-12-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Bone Reports |
| spelling | doaj.art-d42625e9d2854f18b16f079c4b1bd8c22023-12-10T06:16:16ZengElsevierBone Reports2352-18722023-12-0119101664The role of reactive oxygen species in bone cell physiology and pathophysiologyAdriana Marques-Carvalho0Ha-Neui Kim1Maria Almeida2CNC - Center for Neuroscience and Cell Biology, University of Coimbra, UC-Biotech, Biocant Park, Cantanhede, PortugalDivision of Endocrinology and Metabolism, University of Arkansas for Medical Sciences, Little Rock, USA; Center for Musculoskeletal Disease Research, University of Arkansas for Medical Sciences, Little Rock, AR, USADivision of Endocrinology and Metabolism, University of Arkansas for Medical Sciences, Little Rock, USA; Center for Musculoskeletal Disease Research, University of Arkansas for Medical Sciences, Little Rock, AR, USA; Department of Orthopedic Surgery, University of Arkansas for Medical Sciences, Little Rock, USA; Corresponding author at: 4301 W Markham Street, #587, Little Rock, AR 72205, USA.Hydrogen peroxide (H2O2), superoxide anion radical (O2−), and other forms of reactive oxygen species (ROS) are produced by the vast majority of mammalian cells and can contribute both to cellular homeostasis and dysfunction. The NADPH oxidases (NOX) enzymes and the mitochondria electron transport chain (ETC) produce most of the cellular ROS. Multiple antioxidant systems prevent the accumulation of excessive amounts of ROS which cause damage to all cellular macromolecules. Many studies have examined the contribution of ROS to different bone cell types and to skeletal physiology and pathophysiology. Here, we discuss the role of H2O2 and O2− and their major enzymatic sources in osteoclasts and osteoblasts, the fundamentally different ways via which these cell types utilize mitochondrial derived H2O2 for differentiation and function, and the molecular mechanisms that impact and are altered by ROS in these cells. Particular emphasis is placed on evidence obtained from mouse models describing the contribution of different sources of ROS or antioxidant enzymes to bone resorption and formation. Findings from studies using pharmacological or genetically modified mouse models indicate that an increase in H2O2 and perhaps other ROS contribute to the loss of bone mass with aging and estrogen deficiency, the two most important causes of osteoporosis and increased fracture risk in humans.http://www.sciencedirect.com/science/article/pii/S2352187223000128AgingEstrogenFoxOsMitochondriaNOXsOsteoblasts |
| spellingShingle | Adriana Marques-Carvalho Ha-Neui Kim Maria Almeida The role of reactive oxygen species in bone cell physiology and pathophysiology Bone Reports Aging Estrogen FoxOs Mitochondria NOXs Osteoblasts |
| title | The role of reactive oxygen species in bone cell physiology and pathophysiology |
| title_full | The role of reactive oxygen species in bone cell physiology and pathophysiology |
| title_fullStr | The role of reactive oxygen species in bone cell physiology and pathophysiology |
| title_full_unstemmed | The role of reactive oxygen species in bone cell physiology and pathophysiology |
| title_short | The role of reactive oxygen species in bone cell physiology and pathophysiology |
| title_sort | role of reactive oxygen species in bone cell physiology and pathophysiology |
| topic | Aging Estrogen FoxOs Mitochondria NOXs Osteoblasts |
| url | http://www.sciencedirect.com/science/article/pii/S2352187223000128 |
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