Published online Aug 26, 2019. doi: 10.12998/wjcc.v7.i16.2238
Peer-review started: May 7, 2019
First decision: May 31, 2019
Revised: June 23, 2019
Accepted: July 27, 2019
Article in press: July 27, 2019
Published online: August 26, 2019
Processing time: 123 Days and 17.9 Hours
Muscle atrophy and volume reduction in neurogenic congenital clubfoot are the main factors causing limb mobility disorder, which seriously affects the quality of life of children. The rehabilitation treatment of muscle atrophy has great significance. At present, there are few reports on the study of clubfoot muscle atrophy. Therefore, it is of great clinical significance to use effective methods to diagnose and study in-depth mechanism research of clubfoot muscle atrophy.
Until now, the diagnose of clubfoot muscle atrophy is mainly depended on magnetic resonance imaging. Ultrasound is simple and real-time, and it is more suitable for follow-up prenatal observation and postnatal treatment. Therefore, this study clarifies the diagnostic value of 3D tomographic ultrasound imaging (TUI) for neurogenic congenital clubfoot muscle atrophy. There is no targeted drug treatment for clubfoot muscle atrophy currently, so this study attempts to reveal the mechanism of TAZ involvement in clubfoot muscle atrophy and to find drug therapeutic targets.
The objective of this study was to establish an ultrasound evaluation system for clubfoot muscle atrophy and to reveal the possible mechanisms of TAZ and myostatin involvement in clubfoot muscle atrophy and provide a theoretical basis for the development of potential drug therapy.
Prenatal 2D and 3D ultrasound imaging was used to diagnose fetuses with neurological clubfoot. Quantitative evaluation of muscle atrophy was performed by 3D TUI. Muscle specimens were obtained, and protein expression was determined by western blotting and immunostaining. TAZ overexpressed C2C12 cells were differentiated and treated with myostatin, muscle differentiation of each group was compared quantitatively, and the Akt/FOXO4 signaling pathway expression was detected by western blotting.
The 3D TUI can detect the muscle atrophy on the varus side, which is significantly smaller than the contralateral side. In the gastrocnemius specimens, TAZ and myostatin had opposite expression trends and were negatively correlated. Myostatin inhibited C2C12 muscle differentiation, manifested as thinner myotubes, and was rescued by TAZ overexpression. Overexpressed TAZ reduces the increased p-Akt and FOXO4 expression caused by myostatin.
The 3D TUI technology can be used to evaluate neurogenic clubfoot muscle atrophy. TAZ and myostatin expression are negatively correlated in muscle samples. TAZ antagonizes muscle differentiation inhibition induced by myostatin, and the mechanism may potentially work through repression of the Akt/FOXO4 signaling pathway.
Using 3D ultrasound to evaluate the clubfoot muscle atrophy prenatally and postpartum is effective. Appling previously developed TAZ activators for future research in order to develop new drug therapy of clubfoot muscle atrophy is necessary.