About this Research Topic
Duchenne muscular dystrophy (DMD) is a severe X-linked neuromuscular disorder characterized by the absence of dystrophin, a crucial muscle cytoskeletal protein. Predominantly affecting the pediatric population, DMD leads to progressive muscle degeneration due to compromised cell membrane integrity and subsequent cell death. This degeneration is accompanied by chronic inflammation and the production of fibrotic tissue by fibroblasts, which replace healthy muscle tissue over time, severely impacting mobility. Recent studies have also identified cognitive, neurological, and autonomic disorders associated with DMD, suggesting a broader systemic impact. Current therapeutic strategies focus on restoring dystrophin expression or compensating for its absence, with gene therapy and CRISPR/Cas9 editing showing promise. However, challenges remain in effective delivery, sustained expression, and understanding the neural implications of DMD.
While much research has focused on skeletal muscle cells, Duchenne-associated fibroblasts (DAFs) have been relatively understudied, despite their early involvement in fibrosis and potential role in disease progression. Addressing the cellular crosstalk between myocytes and DAFs could provide critical insights into DMD pathophysiology and open new therapeutic avenues.
This Research Topic aims to explore the multifaceted role of Duchenne-associated fibroblasts (DAFs) in DMD, emphasizing their significance alongside myocytes and inflammatory cells. By extending the research focus to include DAFs and their interactions with other cell types, we seek to uncover novel insights into the disease's progression and broaden therapeutic strategies. The research will delve into the potential of fibroblasts to differentiate into various cell types and their role in forming debilitating scar tissue. Additionally, the study aims to enhance our understanding of DMD's impact on the neural system, particularly concerning motor control, and to identify therapeutic molecules that can synergize with genetic and anti-inflammatory therapies.
To gather further insights into the complex interplay of cellular components in DMD, we welcome articles addressing, but not limited to, the following themes:
- Role of DAFs as potential markers in DMD early diagnosis.
- Mechanisms underlying DAFs' altered physiology leading to early-onset profibrotic phenotype.
- Identification of therapeutic molecules with anti-fibrotic action.
- Intersection of gene therapy and anti-inflammatory therapy: current pros and cons and impact on the nervous system.
- Morpho-functional features underlying neurological disorders associated with DMD.
- DAFs’ proteome in DMD versus healthy skeletal myocytes/myoblasts.
- DAFs’ secretome in DMD versus healthy skeletal myocytes/myoblasts.
- Molecular crosstalk between DAFs and myocytes/myoblasts.
- Molecular crosstalk between DAFs and neurons.
- DAFs’ involvement in the DMD brain.
- DAFs’ impact on the DMD nervous system.
- Synergy of gene therapy and anti-fibrotic therapy in DMD animal models.
While much research has focused on skeletal muscle cells, Duchenne-associated fibroblasts (DAFs) have been relatively understudied, despite their early involvement in fibrosis and potential role in disease progression. Addressing the cellular crosstalk between myocytes and DAFs could provide critical insights into DMD pathophysiology and open new therapeutic avenues.
This Research Topic aims to explore the multifaceted role of Duchenne-associated fibroblasts (DAFs) in DMD, emphasizing their significance alongside myocytes and inflammatory cells. By extending the research focus to include DAFs and their interactions with other cell types, we seek to uncover novel insights into the disease's progression and broaden therapeutic strategies. The research will delve into the potential of fibroblasts to differentiate into various cell types and their role in forming debilitating scar tissue. Additionally, the study aims to enhance our understanding of DMD's impact on the neural system, particularly concerning motor control, and to identify therapeutic molecules that can synergize with genetic and anti-inflammatory therapies.
To gather further insights into the complex interplay of cellular components in DMD, we welcome articles addressing, but not limited to, the following themes:
- Role of DAFs as potential markers in DMD early diagnosis.
- Mechanisms underlying DAFs' altered physiology leading to early-onset profibrotic phenotype.
- Identification of therapeutic molecules with anti-fibrotic action.
- Intersection of gene therapy and anti-inflammatory therapy: current pros and cons and impact on the nervous system.
- Morpho-functional features underlying neurological disorders associated with DMD.
- DAFs’ proteome in DMD versus healthy skeletal myocytes/myoblasts.
- DAFs’ secretome in DMD versus healthy skeletal myocytes/myoblasts.
- Molecular crosstalk between DAFs and myocytes/myoblasts.
- Molecular crosstalk between DAFs and neurons.
- DAFs’ involvement in the DMD brain.
- DAFs’ impact on the DMD nervous system.
- Synergy of gene therapy and anti-fibrotic therapy in DMD animal models.
Keywords: Duchenne muscular dystrophy, Duchenne-Associated Fibroblasts, motor control, neuromuscular disease, inflammation, therapeutic molecules
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.
