Abstract
Cerebral palsy is a set of common, severe, motor disabilities categorized by a static, nondegenerative encephalopathy arising in the developing brain and associated with deficits in movement, posture, and activity. Spastic CP, which is the most common type, involves high muscle tone and is associated with altered muscle function including poor muscle growth and contracture, increased extracellular matrix deposition, microanatomic disruption, musculoskeletal deformities, weakness, and difficult movement control. These muscle-related manifestations of CP are major causes of progressive debilitation and frequently require intensive surgical and therapeutic intervention to control. Current clinical approaches involve sophisticated consideration of biomechanics, radiologic assessments, and movement analyses, but outcomes remain difficult to predict. There is a need for more precise and personalized approaches involving omics technologies, data science, and advanced analytics. An improved understanding of muscle involvement in spastic CP is needed. Unfortunately, the fundamental mechanisms and molecular pathways contributing to altered muscle function in spastic CP are only partially understood. In this review, we outline evidence supporting the emerging hypothesis that epigenetic phenomena play significant roles in musculoskeletal manifestations of CP.
Highlights
The goal of most personalized medicine efforts is to provide the right treatment at the right time for every patient. This goal has been elusive for clinicians caring for children with cerebral palsy (CP) due in large part to a lack of understanding of fundamental pathways contributing to disease
Circular RNAs are noncoding RNAs generated by a phenomenon called back splicing which leads to formation of covalently closed circles [167]
Results derived from a PubMed search (((“2010/01/01” [Date-Publication]: “2021/08/01”[DatePublication])) AND ((muscle satellite cells) AND) were included as well; these articles were focused on the role of circular RNAs (circRNA) in regulating the miRNAs
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. The goal of most personalized medicine efforts is to provide the right treatment at the right time for every patient This goal has been elusive for clinicians caring for children with cerebral palsy (CP) due in large part to a lack of understanding of fundamental pathways contributing to disease. CP involve increased muscle stiffness and tone (spasticity), contractures, muscle weakness, and disrupted gait and body positioning [11,14] These motor impairments are frequently accompanied by additional deficits such as intellectual disability, epilepsy, and sensory impairments [15]. Alterations in muscle tissue have been observed in children with CP These include impaired longitudinal growth contributing to contractures [16], decreased muscle crosssectional area [17], increased sarcomere length [13], reduced muscle mass and volume, fibrotic tissue accumulation, increased extracellular matrix, reduced satellite-cell numbers [14], microanatomic disruption of neuromuscular junctions (NMJ) [18], and muscletype-specific alteration of fiber type distributions [19,20]. Identified peer-reviewed, primary journal research articles and reviews published since 2010 are tabulated and discussed in context
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