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Skeletal Homeostasis and Metabolism

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

Deadline for manuscript submissions: closed (20 April 2023) | Viewed by 10055

Special Issue Editor


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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,

The maintenance of bone homeostasis is extremely important for bone health. Pathological or physiological changes, such as aging, inflammation, or estrogen deficiency, lead to increased numbers or activity of osteoclasts as well as a decreased numbers of osteoblasts, tilting the balance in favor of bone resorption and causing bone diseases; however, the molecular mechanisms responsible for imbalances between bone resorption and formation in these conditions are not well understood. This Special Issue will summarize and analyze the research progress of bone metabolism in osteoblasts and osteoclasts as well as osteocytes and gain an in-depth understanding of the key regulatory role of bone metabolism in osteogenesis and osteoclast differentiation and function in the maintenance of bone homeostasis, to provide guidance on the treatment of bone-related diseases such as osteoporosis and to facilitate use of this knowledge on the path to discovering pharmacological targets and new drug therapies. In particular, we welcome research covering novel molecular mechanism, new tools on bone research, or any animal studies with clinical relevance.

Dr. Ha-Neui Kim
Guest Editor

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Keywords

  • metabolism
  • skeletal homeostasis
  • osteoblasts
  • osteoclasts
  • osteoporosis
  • bone
  • aging

Published Papers (4 papers)

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Research

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16 pages, 4050 KiB  
Article
Construction and Analysis of Disuse Atrophy Model of the Gastrocnemius Muscle in Chicken
by Jiawei Mo, Zhijun Wang, Qingchun Liu, Zhenhui Li and Qinghua Nie
Int. J. Mol. Sci. 2022, 23(13), 6892; https://doi.org/10.3390/ijms23136892 - 21 Jun 2022
Cited by 2 | Viewed by 2053
Abstract
Disuse muscle atrophy is identified as the physiological, biochemical, morphological, and functional changes during restricted movement, immobilization, or weightlessness. Although its internal mechanism has been extensively studied in mammals and was thought to be mainly related to oxidative stress, it was unclear whether [...] Read more.
Disuse muscle atrophy is identified as the physiological, biochemical, morphological, and functional changes during restricted movement, immobilization, or weightlessness. Although its internal mechanism has been extensively studied in mammals and was thought to be mainly related to oxidative stress, it was unclear whether it behaved consistently in non-mammals such as chickens. In this study, we tried to construct a disuse atrophy model of the gastrocnemius muscle in chickens by limb immobilization, and collected the gastrocnemius muscles of the fixed group and the control group for RNA sequencing. Through analysis of muscle loss, HE staining, immunohistochemistry, and oxidative stress level, we found that limb immobilization could lead to loss of muscle mass, decrease in muscle fiber diameter, decrease in the proportion of slow muscle fibers, and increase in the proportion of fast muscle fibers, and also cause elevated levels of oxidative stress. In addition, a total of 565 different expression genes (DEGs) were obtained by RNA sequencing, which was significantly enriched in the biological processes such as cell proliferation and apoptosis, reactive oxygen species metabolism, and fast and slow muscle fiber transformation, and it showed that the FOXO signaling pathway, closely related to muscle atrophy, was activated. In brief, we initially confirmed that limb immobilization could induce disuse atrophy of skeletal muscle, and oxidative stress was involved in the process of disuse muscle atrophy. Full article
(This article belongs to the Special Issue Skeletal Homeostasis and Metabolism)
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Review

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17 pages, 1389 KiB  
Review
A Skeletal Muscle-Centric View on Time-Restricted Feeding and Obesity under Various Metabolic Challenges in Humans and Animals
by Christopher Livelo, Yiming Guo and Girish C. Melkani
Int. J. Mol. Sci. 2023, 24(1), 422; https://doi.org/10.3390/ijms24010422 - 27 Dec 2022
Cited by 4 | Viewed by 2475
Abstract
Nearly 50% of adults will suffer from obesity in the U.S. by 2030. High obesity rates can lead to high economic and healthcare burdens in addition to elevated mortality rates and reduced health span in patients. Emerging data demonstrate that obesity is a [...] Read more.
Nearly 50% of adults will suffer from obesity in the U.S. by 2030. High obesity rates can lead to high economic and healthcare burdens in addition to elevated mortality rates and reduced health span in patients. Emerging data demonstrate that obesity is a multifactorial complex disease with various etiologies including aging, a lifestyle of chronic high-fat diets (HFD), genetic predispositions, and circadian disruption. Time-restricted feeding/eating (TRF; TRE in humans) is an intervention demonstrated by studies to show promise as an effective alternative therapy for ameliorating the effects of obesity and metabolic disease. New studies have recently suggested that TRF/TRE modulates the skeletal muscle which plays a crucial role in metabolism historically observed to be impaired under obesity. Here we discuss recent findings regarding potential mechanisms underlying TRF’s modulation of skeletal muscle function, metabolism, and structure which may shed light on future research related to TRF as a solution to obesity. Full article
(This article belongs to the Special Issue Skeletal Homeostasis and Metabolism)
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15 pages, 3439 KiB  
Review
Osteopathy in Complex Lymphatic Anomalies
by Ernesto Solorzano, Andrew L. Alejo, Hope C. Ball, Joseph Magoline, Yusuf Khalil, Michael Kelly and Fayez F. Safadi
Int. J. Mol. Sci. 2022, 23(15), 8258; https://doi.org/10.3390/ijms23158258 - 26 Jul 2022
Cited by 5 | Viewed by 2617
Abstract
Complex Lymphatic Anomalies (CLA) are lymphatic malformations with idiopathic bone and soft tissue involvement. The extent of the abnormal lymphatic presentation and boney invasion varies between subtypes of CLA. The etiology of these diseases has proven to be extremely elusive due to their [...] Read more.
Complex Lymphatic Anomalies (CLA) are lymphatic malformations with idiopathic bone and soft tissue involvement. The extent of the abnormal lymphatic presentation and boney invasion varies between subtypes of CLA. The etiology of these diseases has proven to be extremely elusive due to their rarity and irregular progression. In this review, we compiled literature on each of the four primary CLA subtypes and discuss their clinical presentation, lymphatic invasion, osseous profile, and regulatory pathways associated with abnormal bone loss caused by the lymphatic invasion. We highlight key proliferation and differentiation pathways shared between lymphatics and bone and how these systems may interact with each other to stimulate lymphangiogenesis and cause bone loss. Full article
(This article belongs to the Special Issue Skeletal Homeostasis and Metabolism)
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Other

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8 pages, 1822 KiB  
Opinion
Osteoporosis in Light of a New Mechanism Theory of Delayed Onset Muscle Soreness and Non-Contact Anterior Cruciate Ligament Injury
by Balázs Sonkodi, Rita Bardoni and Gyula Poór
Int. J. Mol. Sci. 2022, 23(16), 9046; https://doi.org/10.3390/ijms23169046 - 12 Aug 2022
Cited by 9 | Viewed by 2337
Abstract
Osteoporosis is a disorder, with a largely unknown pathomechanism, that is often marked as a “silent thief”, because it usually only becomes undisguised when fractures occur. This implies that the pathological damage occurs earlier than the sensation of pain. The current authors put [...] Read more.
Osteoporosis is a disorder, with a largely unknown pathomechanism, that is often marked as a “silent thief”, because it usually only becomes undisguised when fractures occur. This implies that the pathological damage occurs earlier than the sensation of pain. The current authors put forward a non-contact injury model in which the chronic overloading of an earlier autologously microinjured Piezo2 ion channel of the spinal proprioceptor terminals could lead the way to re-injury and earlier aging in a dose-limiting and threshold-driven way. As a result, the aging process could eventually lead the way to the metabolic imbalance of primary osteoporosis in a quad-phasic non-contact injury pathway. Furthermore, it is emphasised that delayed onset muscle soreness, non-contact anterior cruciate injury and osteoporosis could have the same initiating proprioceptive non-contact Piezo2 channelopathy, at different locations, however, with different environmental risk factors and a different genetic predisposition, therefore producing different outcomes longitudinally. The current injury model does not intend to challenge any running pathogenic theories or findings, but rather to highlight a principal injury mechanism. Full article
(This article belongs to the Special Issue Skeletal Homeostasis and Metabolism)
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