Author(s) :

Yiwen Evan Sun.

Volume/Issue :

Abstract :

Fibrosis-induced skeletal muscle atrophy, driven by excessive extracellular matrix (ECM) deposition and abnormal collagen accumulation, represents a critical barrier to muscle regeneration. MicroRNA-29 (miR-29) has been shown to effectively suppress fibrosis by directly targeting collagen synthesis genes, such as COL1A1 and COL3A1, while preserving key ECM components like laminin and fibronectin. While various delivery methods have been explored, including Adeno-associated viruses (AAVs), nanoparticles, lipid-based transfection reagents, and electroporification, off-target effects remain a significant challenge. Preclinical studies have demonstrated the efficacy of miR-29, particularly when combined with other therapies, in reducing collagen deposition and restoring gastrocnemius muscle strength in murine models, offering preliminary success for miR-29 in treating skeletal muscle disorders like Duchenne muscular dystrophy. Nevertheless, the limited translation to success in clinical trials reflects the technology’s ongoing challenges in targeted delivery, safety, and dosage optimization. This paper provides updates on the current state of the literature on the use of miR-29. The results underscore the need for further research to overcome these barriers, particularly in the context of skeletal muscle fibrosis, to fully unlock the therapeutic potential of miR-29.