August is Spinal Muscular Atrophy (SMA) Awareness Month, a time dedicated to increasing understanding and support for those affected by this debilitating genetic condition. Emerging research highlights the relevant role of High-Mobility Group Box 1 (HMGB1) in muscular diseases, offering new insights that could inform future therapeutic strategies for SMA.
HMGB1 and Skeletal Muscle Regeneration
Recent studies have illuminated how HMGB1 impedes skeletal muscle regeneration.
HMGB1 inhibits Pax-7 synthesis, a crucial factor for myogenic differentiation, by increasing the expression of miR-342-5p through RAGE, TLR2, TLR4, and c-Src signaling pathways. The therapeutic inhibition of HMGB1 protein in a mouse model demonstrated the rescue of Pax-7 expression and muscle regeneration, suggesting that targeting the HMGB1/Pax-7 axis could promote muscle regeneration in SMA patients.
HMGB1 and Muscle Atrophy
Another study found that HMGB1 promotes skeletal muscle atrophy through an IL-18-dependent mechanism. HMGB1-induced increases in IL-18 levels were shown to enhance the expression of muscle atrophy markers while inhibiting myogenic markers. This process involved the RAGE/p85/Akt/mTOR/c-Jun signaling pathway. The use of HMGB1 shRNA to suppress HMGB1 and IL-18 signaling successfully rescued muscle-specific differentiation markers in cell and mouse models, indicating that the HMGB1/IL-18 axis is a promising target for treating muscle atrophy in SMA.
These findings underscore the potential of HMGB1 as both a biomarker and a therapeutic target in managing SMA. New treatments may be developed to mitigate muscle atrophy and enhance muscle regeneration, improving the quality of life for SMA patients.
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Read the full articles about the studies:
https://pubmed.ncbi.nlm.nih.gov/36497194/
https://pubmed.ncbi.nlm.nih.gov/37963838/
