Degenerative musculoskeletal diseases (DMDs)have a considerable impact on patient morbidity and mortality, leading to a significant burden on society. Patients with DMDs often suffer from pain, a decline in function, and reduced exercise capacity, leading to long-term or permanent limitations in their ability to carry out daily activities. Skeletal muscle accounts for 40% of body mass and undergoes structural and functional changes as we age. After the age of 50, the human body loses an average of 15-30% of muscle mass each decade, along with a sharp decline in muscle strength. As a result of diffuse muscle wasting and loss of strength, sarcopenia not only decreases the quality of life of the elderly but also leads to a major medical burden. Despite this, there is currently no approved and effective therapy aimed at delaying or reversing sarcopenia.
Musculoskeletal degeneration represents the most drastic and significant change that occurs during the aging process. Despite the growing concern to address this issue in aging interventions, most studies tend to focus solely on observing the degenerative clinical phenomena, with little attention given to the examination of the specific cellular mechanisms of degeneration. Cellular senescence is characterized as an irreversible cell cycle arrest resulting from persistent exogenous and endogenous stress causing damage to the cells. Senescent cells are typical products of cellular aging with specific biological properties and functions. Studies conducted recently have shown that senescent cells play a significant role in musculoskeletal degeneration, with their presence increasing rapidly in degenerative skeletal muscles. Although treatment strategies involving rapamycin, dimethyldigua, and dasatinib + quercetin, have been proposed to combat this degeneration by targeting senescent cells, further extensive research is still needed to develop effective solutions and applications. Further understanding of the molecular mechanisms of cellular senescence in musculoskeletal diseases will provide exciting new insights into the understanding and prevention of musculoskeletal degeneration.
This Research Topic aims to initiate research and discussions into the etiology, molecular regulation mechanisms, potential solutions and therapeutic tools related to musculoskeletal degeneration. Our primary focus will be on exploring the issue related to aging in this field. Therefore, we welcome submissions of Original Research articles and Reviews regarding musculoskeletal degeneration that focus on, but are not limited to, the following aspects:
1. Basic and clinical research on DMDs, such as osteoporosis, osteoarthritis, osteonecrosis, and other related diseases;
2. Examine the potential cellular mechanisms involved in regulating musculoskeletal metabolism;
3. To investigate the relevant role played by cellular senescence in musculoskeletal degeneration and the progress of aging-related signaling pathways;
4. Identify potential protein targets that could be used for the treatment of musculoskeletal degeneration;
5. Identify and evaluate potential clinical drugs and the underlying mechanisms that affect musculoskeletal degeneration.
Degenerative musculoskeletal diseases (DMDs)have a considerable impact on patient morbidity and mortality, leading to a significant burden on society. Patients with DMDs often suffer from pain, a decline in function, and reduced exercise capacity, leading to long-term or permanent limitations in their ability to carry out daily activities. Skeletal muscle accounts for 40% of body mass and undergoes structural and functional changes as we age. After the age of 50, the human body loses an average of 15-30% of muscle mass each decade, along with a sharp decline in muscle strength. As a result of diffuse muscle wasting and loss of strength, sarcopenia not only decreases the quality of life of the elderly but also leads to a major medical burden. Despite this, there is currently no approved and effective therapy aimed at delaying or reversing sarcopenia.
Musculoskeletal degeneration represents the most drastic and significant change that occurs during the aging process. Despite the growing concern to address this issue in aging interventions, most studies tend to focus solely on observing the degenerative clinical phenomena, with little attention given to the examination of the specific cellular mechanisms of degeneration. Cellular senescence is characterized as an irreversible cell cycle arrest resulting from persistent exogenous and endogenous stress causing damage to the cells. Senescent cells are typical products of cellular aging with specific biological properties and functions. Studies conducted recently have shown that senescent cells play a significant role in musculoskeletal degeneration, with their presence increasing rapidly in degenerative skeletal muscles. Although treatment strategies involving rapamycin, dimethyldigua, and dasatinib + quercetin, have been proposed to combat this degeneration by targeting senescent cells, further extensive research is still needed to develop effective solutions and applications. Further understanding of the molecular mechanisms of cellular senescence in musculoskeletal diseases will provide exciting new insights into the understanding and prevention of musculoskeletal degeneration.
This Research Topic aims to initiate research and discussions into the etiology, molecular regulation mechanisms, potential solutions and therapeutic tools related to musculoskeletal degeneration. Our primary focus will be on exploring the issue related to aging in this field. Therefore, we welcome submissions of Original Research articles and Reviews regarding musculoskeletal degeneration that focus on, but are not limited to, the following aspects:
1. Basic and clinical research on DMDs, such as osteoporosis, osteoarthritis, osteonecrosis, and other related diseases;
2. Examine the potential cellular mechanisms involved in regulating musculoskeletal metabolism;
3. To investigate the relevant role played by cellular senescence in musculoskeletal degeneration and the progress of aging-related signaling pathways;
4. Identify potential protein targets that could be used for the treatment of musculoskeletal degeneration;
5. Identify and evaluate potential clinical drugs and the underlying mechanisms that affect musculoskeletal degeneration.
