Key result
Genetic ablation of nrap in nebulin deficiency restored sarcomeric disorganization, reduced protein aggregates, and improved skeletal muscle function in a zebrafish model of nemaline myopathy.
Why the study?
Nemaline myopathy lacks a cure and nebulin gene therapies are challenging, making targeting disease modifiers an attractive therapeutic strategy.
Does genetic ablation of nrap improve skeletal muscle structure and function in a zebrafish model of nebulin deficiency?
Does genetic ablation of nrap improve skeletal muscle structure and function in a zebrafish model of nebulin deficiency?
Genetic ablation of nrap rescues sarcomere defects and improves muscle function in a zebrafish model of nebulin-related nemaline myopathy, suggesting Nrap as a potential therapeutic target.
Nrap ablation merits further preclinical study in nemaline myopathy; leaves open translation and human therapeutic potential.
Nemaline myopathy (NM) is a rare neuromuscular disorder associated with congenital or childhood-onset of skeletal muscle weakness and hypotonia, which results in limited motor function. NM is a genetic disorder and mutations in 12 genes are known to contribute to autosomal dominant or recessive forms of the disease. Recessive mutations in nebulin (NEB) are the most common cause of NM affecting about 50% of patients. Because of the large size of the NEB gene and lack of mutational hot spots, developing therapies that can benefit a wide group of patients is challenging. Although there are several promising therapies under investigation, there is no cure for NM. Therefore, targeting disease modifiers that can stabilize or improve skeletal muscle function may represent alternative therapeutic strategies. Our studies have identified Nrap upregulation in nebulin deficiency that contributes to structural and functional deficits in NM. We show that genetic ablation of nrap in nebulin deficiency restored sarcomeric disorganization, reduced protein aggregates and improved skeletal muscle function in zebrafish. Our findings suggest that Nrap is a disease modifier that affects skeletal muscle structure and function in NM; thus, therapeutic targeting of Nrap in nebulin-related NM and related diseases may be beneficial for patients.
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Casey et al. (2023) studied Nebulin-related nemaline myopathy. Genetic ablation of nrap was evaluated on Sarcomeric disorganization, protein aggregates, and skeletal muscle function. Genetic ablation of nrap in nebulin deficiency restored sarcomeric disorganization, reduced protein aggregates, and improved skeletal muscle function in a zebrafish model of nemaline myopathy.
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