Anti-inflammatory cytokines (e.g., IL-10) |
Endogenous molecules; deactivate proinflammatory macrophages and induce the anti-inflammatory phenotype |
Short-term effect; nonspecific (could directly impair other cellular processes in skeletal muscle regeneration) |
[115, 117] |
Growth factors (e.g., IGF-1) |
Endogenous molecules; promote macrophage transition to their anti-inflammatory phenotype; promote muscle growth |
Short-term effect; systemic side effects |
[121, 124, 125] |
RNA silencing (e.g., miRNA, siRNA) |
Specifically target genes implicated in chronic inflammation; skewed macrophages toward pro- or anti-inflammatory phenotype |
Poor stability; inappropriate distribution; off-target side effects; delivery |
[126, 127, 136, 138, 200] |
NF-κB inhibitors |
Dampen inflammation; easy to deliver; good stability |
Nonspecific (could directly impair other cellular processes in skeletal muscle regeneration) |
[143] |
Nutritional compounds (proteins, amino acids, PUFA, vitamins, and antioxidants) |
Promote macrophage transition; potentiate the effect of other therapies; inexpensive; easy to administer |
Mild therapeutic effect |
[166, 171, 172] |
Biomaterials |
Skewed macrophages toward pro- or anti-inflammatory phenotype; local effects; long-term effects; combination with other therapies |
Invasive; biocompatibility; risk of contamination; degradation of the biomaterial |
[201] |
Macrophage transplantation |
Specifically deliver the desired macrophage subset; increase the success rate of satellite cell transplantation |
Invasive; systemic side effects; expensive; time consuming |
[193–195] |