About this Research Topic
Musculoskeletal diseases are a public health problem, and their incidence is increasing which contributes to the huge social and economic burden to the worldwide. These diseases include intervertebral disc degeneration, paraspinal muscle degeneration, osteoarthritis, ankylosing spondylitis, rheumatoid arthritis, osteosarcoma, sacropenia and scoliosis, and osteoporosis. Despite the prevalence of these diseases, the current treatment for musculoskeletal diseases have not achieved satisfactory results. Therefore, novel therapeutics have to be developed.
Cell death (such as cuproptosis, ferroptosis, pyroptosis, apoptosis), oxidative stress and inflammatory responses are the key pathomechanisms. Moreover, accumulating evidence has demonstrated that cuproptosis, ferroptosis, pyroptosis, and oxidative stress are closely associated with inflammatory responses. Similarly, pro-inflammatory factors can also cause a variety of cell deaths and oxidative stress. Addiionally, cuproptosis and ferroptosis can promote oxidative stress and the production of reactive oxygen species. Besides, non-coding RNA and genes are widely involved in the regulation of cell death, oxidative stress, and inflammatory responses, thereby regulating the progression of musculoskeletal diseases. Thus, further studies on the role and mechanism of cells death, oxidative stress and inflammatory response in musculoskeletal diseases are promising and necessary as they could shed light on novel therapeutics such as targeted molecular gene therapy.
The purpose of this Research Topic is to provide a platform for researchers to investigate the role and pathological mechanism of cells death, oxidative stress and inflammatory responses in musculoskeletal diseases. In particular, we welcome submissions of Original Basic Research, Translational Research and Reviews exploring this research topic. In addition, we also welcome research regarding non-coding RNA and genes participant in mediating cell death, oxidative stress, and inflammatory responses, and musculoskeletal diseases using bioinformatics analysis and single cell sequencing analysis methods.
We welcome papers that cover but are not limited to the following areas:
1. The role and mechanisms of cell death, oxidative stress and inflammatory responses in osteoarthritis, ankylosing spondylitis and rheumatoid arthritis;
2. The role and mechanisms of cell death, oxidative stress and inflammatory responses in intervertebral disc degeneration and paraspinal muscle degeneration, and spinal cord injury;
3. The role and mechanisms of cell death, oxidative stress and inflammatory responses in osteosarcoma, sacropenia, scoliosis, and osteoporosis;
4. Research on bioinformatics analysis and single cell sequencing analysis methods related to non-coding RNA and genes-mediated cells death, oxidative stress and inflammatory response in musculoskeletal diseases
5. Specific molecular signaling pathways underlying oxidative stress-induced musculoskeletal diseases；
6. Potential therapeutic molecules to treat musculoskeletal diseases.
7. Animal models induced by oxidative stress in musculoskeletal diseases.
Cell death (such as cuproptosis, ferroptosis, pyroptosis, apoptosis), oxidative stress and inflammatory responses are the key pathomechanisms. Moreover, accumulating evidence has demonstrated that cuproptosis, ferroptosis, pyroptosis, and oxidative stress are closely associated with inflammatory responses. Similarly, pro-inflammatory factors can also cause a variety of cell deaths and oxidative stress. Addiionally, cuproptosis and ferroptosis can promote oxidative stress and the production of reactive oxygen species. Besides, non-coding RNA and genes are widely involved in the regulation of cell death, oxidative stress, and inflammatory responses, thereby regulating the progression of musculoskeletal diseases. Thus, further studies on the role and mechanism of cells death, oxidative stress and inflammatory response in musculoskeletal diseases are promising and necessary as they could shed light on novel therapeutics such as targeted molecular gene therapy.
The purpose of this Research Topic is to provide a platform for researchers to investigate the role and pathological mechanism of cells death, oxidative stress and inflammatory responses in musculoskeletal diseases. In particular, we welcome submissions of Original Basic Research, Translational Research and Reviews exploring this research topic. In addition, we also welcome research regarding non-coding RNA and genes participant in mediating cell death, oxidative stress, and inflammatory responses, and musculoskeletal diseases using bioinformatics analysis and single cell sequencing analysis methods.
We welcome papers that cover but are not limited to the following areas:
1. The role and mechanisms of cell death, oxidative stress and inflammatory responses in osteoarthritis, ankylosing spondylitis and rheumatoid arthritis;
2. The role and mechanisms of cell death, oxidative stress and inflammatory responses in intervertebral disc degeneration and paraspinal muscle degeneration, and spinal cord injury;
3. The role and mechanisms of cell death, oxidative stress and inflammatory responses in osteosarcoma, sacropenia, scoliosis, and osteoporosis;
4. Research on bioinformatics analysis and single cell sequencing analysis methods related to non-coding RNA and genes-mediated cells death, oxidative stress and inflammatory response in musculoskeletal diseases
5. Specific molecular signaling pathways underlying oxidative stress-induced musculoskeletal diseases；
6. Potential therapeutic molecules to treat musculoskeletal diseases.
7. Animal models induced by oxidative stress in musculoskeletal diseases.
Keywords: Inflammation, Cell Death, Cuproptosis, Ferroptosis, Pyroptosis, Apoptosis, Intervertebral Disc Degeneration, Paraspinal Muscle Degeneration
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
