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Effects of Metabolic Syndrome and Aging on Metabolic Changes in the Musculoskeletal System

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 3215

Special Issue Editors


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Guest Editor
1. Department of Physical Education, Gyeongsang National University, Jinju 660701, Republic of Korea
2. Research Institute of Pharmaceutical Sciences, Gyeongsang National University, Jinju 660-701, Republic of Korea
Interests: aging; metabolic syndrome; immune function; genomics

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Guest Editor
Biomedical Research Institute, Gyeongsang National University Hospital, Jinju 52727, Republic of Korea
Interests: osteoarthritis; sarcopenia; osteoporosis

Special Issue Information

Dear Colleagues,

Aging itself is a risk factor for metabolic syndrome and vice versa. Those two risk factors share close relationships and are directly related to the quality of life. In particular, a functional decline in the musculoskeletal system related to physical movement is an important factor that degrades the quality of life. Therefore, the recent global aging trend and the worldwide increase in the obese population are making it difficult to maintain the homeostasis of the musculoskeletal system of many individuals, and interest in this is increasing daily. This Special Issue aims to provide readers with important molecular biological insights into the adverse effects of metabolic syndrome and aging on the musculoskeletal system and how to improve them.

As the Guest Editors of “Effects of Metabolic Syndrome and Aging on Metabolic Changes in the Musculoskeletal System”, we invite you to submit your manuscript to Current Issues in Molecular Biology. We welcome experimental research, systematic review and meta-analyses, and narrative reviews related to this topic.

Dr. Kyung-Wan Baek
Dr. Youn-Kwan Jung
Guest Editors

Manuscript Submission Information

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Keywords

  • skeletal muscle
  • bone
  • metabolic syndrome
  • osteoporosis
  • sarcopenia
  • osteoarthritis

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Published Papers (2 papers)

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Research

10 pages, 12264 KiB  
Communication
Adipose Tissue Macrophage Polarization Is Altered during Recovery after Exercise: A Large-Scale Flow Cytometric Study
by Kyung-Wan Baek, Ji Hyun Kim, Hak Sun Yu and Ji-Seok Kim
Curr. Issues Mol. Biol. 2024, 46(2), 1308-1317; https://doi.org/10.3390/cimb46020083 - 2 Feb 2024
Viewed by 1347
Abstract
We performed a large-scale flow cytometric analysis to determine whether M1 macrophage (M1Ø) and M2 macrophage (M2Ø) polarization in white adipose tissue (WAT) was altered immediately after exercise. Additionally, we comprehensively investigated the effects of obesity, exercise intensity, and recovery time on macrophage [...] Read more.
We performed a large-scale flow cytometric analysis to determine whether M1 macrophage (M1Ø) and M2 macrophage (M2Ø) polarization in white adipose tissue (WAT) was altered immediately after exercise. Additionally, we comprehensively investigated the effects of obesity, exercise intensity, and recovery time on macrophage polarization in WAT. A single exercise bout of various intensities (ND, non-exercise control; -LIE, low-intensity exercise; -MIE, mid-intensity exercise; -HIE, high-intensity exercise) was performed by normal mice (ND) and obese mice (HFD). To confirm differences in M1Ø/M2Ø polarization in WAT based on the recovery time after a single exercise bout, WAT was acquired at 2 h, 24 h, and 48 h after exercise (total n = 168, 7 mice × 4 groups × 2 diets × 3 recovery time). The harvested WAT was immediately analyzed by flow cytometry, and macrophages were fluorescently labeled using F4/80, as well as M1Ø with CD11c and M2Øs with CD206. After a single bout of exercise, the M2Ø/M1Ø polarization ratio of WAT increases in both normal and obese mice, but differences vary depending on recovery time and intensity. Regardless of obesity, our findings showed that there could be a transient increase in M1Ø in WAT over a short recovery time (24 h) post-exercise (in ND-MIE, ND-HIE, and HFD-HIE). Furthermore, it was observed that the greater the exercise intensity in obese mice, the more effective the induction of M2Ø polarization immediately after exercise, as well as the maintenance of high M2Ø polarization, even after a prolonged recovery time. Full article
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12 pages, 1977 KiB  
Article
Verbascoside Inhibits/Repairs the Damage of LPS-Induced Inflammation by Regulating Apoptosis, Oxidative Stress, and Bone Remodeling
by Sahika Pinar Akyer, Ege Rıza Karagur, Melek Tunc Ata, Emine Kilic Toprak, Aysegul Cort Donmez and Baris Ozgur Donmez
Curr. Issues Mol. Biol. 2023, 45(11), 8755-8766; https://doi.org/10.3390/cimb45110550 - 31 Oct 2023
Cited by 1 | Viewed by 1451
Abstract
Osteocytes play an important role as regulators of both osteoclasts and osteoblasts, and some proteins that are secreted from them play a role in bone remodeling and modeling. LPS affects bone structure because it is an inflammatory factor, despite verbascoside’s potential for bone [...] Read more.
Osteocytes play an important role as regulators of both osteoclasts and osteoblasts, and some proteins that are secreted from them play a role in bone remodeling and modeling. LPS affects bone structure because it is an inflammatory factor, despite verbascoside’s potential for bone preservation and healing. Osteocytes may also be involved in the control of the bone’s response to immunological changes in inflammatory situations. MLO-Y4 cells were cultured in either supplemented -MEM alone with a low serum to inhibit cell growth or media with LPS (10 ng/mL) and/or verbascoside (50 g/mL) to show the LPS effect. In our research, LPS treatment increased RANKL levels while decreasing OPG and RUNX2 expression. Treatment with verbascoside reduced RANKL expression. In our work, verbascoside increased the expression of OPG and RUNX2. In MLO-Y4 cells exposed to verbascoside, SOD, CAT, and GSH activities as well as the expression levels of bone mineralization proteins like PHEX, RUNX2, and OPG were all elevated. Full article
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