7 March 2024 | Mikhail V. Dubinin, Irina B. Mikheeva, Anastasia E. Stepanova, Anastasia D. Igoshkina, Alena A. Cherepanova, Alena A. Semenova, Vyacheslav A. Sharapov, Igor I. Kireev, Konstantin N. Belosludtsev
This study investigates the therapeutic potential of mitochondrial transplantation therapy (MTT) in Duchenne muscular dystrophy (DMD) model mice, specifically mdx mice. DMD is characterized by the loss of dystrophin protein, leading to mitochondrial dysfunction and muscle fiber instability. The researchers applied MTT by injecting allogeneic mitochondria from healthy animals into the hind limbs of mdx mice. The results showed that MTT alleviated skeletal muscle injury, reduced calcium deposits and serum creatine kinase levels, and improved grip strength and motor activity in the recipient mdx mice. The mitochondrial ultrastructure and sarcoplasmic reticulum/mitochondria interactions were normalized in mdx muscles, while oxidative phosphorylation efficiency and lipid peroxidation products were reduced. MTT did not affect the expression of mitochondrial signature genes or mtDNA levels. The study concludes that systemic MTT mitigates destructive processes in the quadriceps muscle of mdx mice, suggesting its potential as a therapeutic approach for DMD. However, further research is needed to explore the long-term effects and optimal methods of MTT administration.This study investigates the therapeutic potential of mitochondrial transplantation therapy (MTT) in Duchenne muscular dystrophy (DMD) model mice, specifically mdx mice. DMD is characterized by the loss of dystrophin protein, leading to mitochondrial dysfunction and muscle fiber instability. The researchers applied MTT by injecting allogeneic mitochondria from healthy animals into the hind limbs of mdx mice. The results showed that MTT alleviated skeletal muscle injury, reduced calcium deposits and serum creatine kinase levels, and improved grip strength and motor activity in the recipient mdx mice. The mitochondrial ultrastructure and sarcoplasmic reticulum/mitochondria interactions were normalized in mdx muscles, while oxidative phosphorylation efficiency and lipid peroxidation products were reduced. MTT did not affect the expression of mitochondrial signature genes or mtDNA levels. The study concludes that systemic MTT mitigates destructive processes in the quadriceps muscle of mdx mice, suggesting its potential as a therapeutic approach for DMD. However, further research is needed to explore the long-term effects and optimal methods of MTT administration.