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Quality Control of Mitochondria: Protection against Bone Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Role of Xenobiotics".

Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 2121

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Guest Editor
Center for Musculoskeletal Disease Research and Center for Osteoporosis and Metabolic Bone Diseases, Department of Internal Medicine, Division of Endocrinology and Metabolism, University of Arkansas for Medical Sciences, 4301 W. Markham Street, Little Rock, AR 72205-7199, USA
Interests: osteoclasts; osteoblasts; osteocytes; mitochondrial quality control; osteoporosis; aging; cellular senescence; oxidative stress
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Special Issue Information

Dear Colleagues,

A balance between the function of bone-resorbing osteoclasts and bone-building osteoblasts is essential for bone homeostasis. However, pathological or physiological changes, such as IRE, inflammation, or aging, lead to increased osteoclast numbers and decreased osteoblast numbers, tilting the balance in favor of bone resorption and eventually causing bone diseases. Thus, understanding the cellular and molecular mechanisms involved in the differentiation of the two types of bone cells is important for the development of novel therapies.

Mitochondria are dynamic organelles whose structure is constantly changing via several processes that include fusion and fission of the tubular mitochondrial network, mitochondrial biogenesis, and elimination of unwanted mitochondria by mitophagy (mitochondrial specific autophagy). Maintaining a healthy mitochondria network is vital for fatty acid oxidation, oxidative phosphorylation (OxPhos), and energy production, among many other metabolic functions. OxPhos produces mitochondrial ROS as byproducts, which can be important signaling molecules but, when produced in excess, damage cells and contribute to disease and aging.

We invite researchers to submit original research and review articles covering significant developments in the mitochondrial function and oxidative stress of bone cells, as well as novel medicines or strategies that hold promise in the prevention and/or treatment of skeletal diseases. In particular, we welcome research covering novel molecular mechanisms, new tools on bone research, or any animal studies with clinical relevance.

Dr. Ha-Neui Kim
Guest Editor

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Keywords

  • Osteoclast
  • Osteoblast
  • osteocyte
  • chondrocyte
  • ROS
  • mitochondria
  • skeletal diseases
  • aging

Published Papers (1 paper)

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Research

17 pages, 3200 KiB  
Article
Ionizing Radiation Activates Mitochondrial Function in Osteoclasts and Causes Bone Loss in Young Adult Male Mice
by Kimberly K. Richardson, Wen Ling, Kimberly Krager, Qiang Fu, Stephanie D. Byrum, Rupak Pathak, Nukhet Aykin-Burns and Ha-Neui Kim
Int. J. Mol. Sci. 2022, 23(2), 675; https://doi.org/10.3390/ijms23020675 - 8 Jan 2022
Cited by 9 | Viewed by 1873
Abstract
The damaging effects of ionizing radiation (IR) on bone mass are well-documented in mice and humans and are most likely due to increased osteoclast number and function. However, the mechanisms leading to inappropriate increases in osteoclastic bone resorption are only partially understood. Here, [...] Read more.
The damaging effects of ionizing radiation (IR) on bone mass are well-documented in mice and humans and are most likely due to increased osteoclast number and function. However, the mechanisms leading to inappropriate increases in osteoclastic bone resorption are only partially understood. Here, we show that exposure to multiple fractions of low-doses (10 fractions of 0.4 Gy total body irradiation [TBI]/week, i.e., fractionated exposure) and/or a single exposure to the same total dose of 4 Gy TBI causes a decrease in trabecular, but not cortical, bone mass in young adult male mice. This damaging effect was associated with highly activated bone resorption. Both osteoclast differentiation and maturation increased in cultures of bone marrow-derived macrophages from mice exposed to either fractionated or singular TBI. IR also increased the expression and enzymatic activity of mitochondrial deacetylase Sirtuin-3 (Sirt3)—an essential protein for osteoclast mitochondrial activity and bone resorption in the development of osteoporosis. Osteoclast progenitors lacking Sirt3 exposed to IR exhibited impaired resorptive activity. Taken together, targeting impairment of osteoclast mitochondrial activity could be a novel therapeutic strategy for IR-induced bone loss, and Sirt3 is likely a major mediator of this effect. Full article
(This article belongs to the Special Issue Quality Control of Mitochondria: Protection against Bone Diseases)
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