The regenerative potential of Pax3/Pax7 on skeletal muscle injury

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Background Skeletal muscle mishaps are the most well-known incidents in society, especially among athletes and the military population. From the various urgency, this accident needs to be cured more quickly. However, the current treatment still has some shortcomings and is less effective. In this case, Paired box 3 and Paired box 7 (Pax3/Pax7) proteins that induce stem cells could potentially be an alternative treatment for skeletal muscle injuries. This paper aimed to analyse the potential treatment of Pax3/Pax7 proteins inducing the stem cell for skeletal muscle injuries. We did a narrative review by gathering several scientific journals from several leading platforms like PubMed and Scopus. As common accidents, skeletal muscle disease could be due to workplace and non-workplace causes. The highest risk occurs in the athlete and military environment. The treatment of current skeletal muscle injuries is protection, rest, ice, compression, and elevation (PRICE), non-steroidal anti-inflammatory drugs (NSAIDs), and mechanical stimulation. However, it is considered less effective, especially in NSAIDs, inhibiting myogenic cell proliferation. The current finding indicates that the stem cells have markers known as Pax3/Pax7. The role of both markers in muscle injury, Pax3/Pax7, as transcription factors will induce cell division by H3K4 methylation mechanisms and chromatin modificati

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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