Mitochondrial transplantation therapy (MTT) improves muscular dystrophy in mdx mice. The study used allogeneic mitochondria from healthy mice injected into the hind limbs of mdx mice, leading to reduced skeletal muscle injury, calcium deposits, and creatine kinase levels, along with improved grip strength and motor activity. Mitochondrial ultrastructure and sarcoplasmic reticulum/mitochondria interactions were normalized, while oxidative phosphorylation efficiency and lipid peroxidation were reduced. MTT did not affect mitochondrial signature genes or mtDNA levels. MTT alleviated destructive processes in quadriceps muscles of mdx mice. The therapy showed no significant effect on inflammatory cytokine expression, suggesting minimal immune response. MTT improved muscle strength and motor activity, with significant effects on hind limb function. Mitochondrial function parameters, including respiration and calcium handling, were improved. MTT reduced MDA levels, indicating lower oxidative stress. MTT did not alter mitochondrial gene expression or mtDNA levels. The study highlights MTT as a potential therapeutic approach for Duchenne muscular dystrophy. However, further research is needed to understand the mechanisms and long-term effects of MTT. The study also notes limitations, including the need for more detailed control group comparisons and further investigation into the effects of MTT on different tissues and ages.Mitochondrial transplantation therapy (MTT) improves muscular dystrophy in mdx mice. The study used allogeneic mitochondria from healthy mice injected into the hind limbs of mdx mice, leading to reduced skeletal muscle injury, calcium deposits, and creatine kinase levels, along with improved grip strength and motor activity. Mitochondrial ultrastructure and sarcoplasmic reticulum/mitochondria interactions were normalized, while oxidative phosphorylation efficiency and lipid peroxidation were reduced. MTT did not affect mitochondrial signature genes or mtDNA levels. MTT alleviated destructive processes in quadriceps muscles of mdx mice. The therapy showed no significant effect on inflammatory cytokine expression, suggesting minimal immune response. MTT improved muscle strength and motor activity, with significant effects on hind limb function. Mitochondrial function parameters, including respiration and calcium handling, were improved. MTT reduced MDA levels, indicating lower oxidative stress. MTT did not alter mitochondrial gene expression or mtDNA levels. The study highlights MTT as a potential therapeutic approach for Duchenne muscular dystrophy. However, further research is needed to understand the mechanisms and long-term effects of MTT. The study also notes limitations, including the need for more detailed control group comparisons and further investigation into the effects of MTT on different tissues and ages.