Abstrait

Cardiomyocytes Increase in Transmitting Tissue Due to Congenital Arteritis

Kim Gyun

The etiology of MMA is still unknown. The onset of disease in a large number of pediatric cases raises the question of the role of genetic factors in disease etiology. The clinical course or progression of MMA is largely unknown in these patients. By building comprehensive molecular and cellular profiles of pediatric MMA patients’ plasma and CSF, respectively, our study provides insight into the levels of circulating endothelial progenitor cells (cEPCs) and the pathogenesis of MMA and the selection of early stages of the disease. The aim is to elucidate the release of proteins that have been induced-progression. Cytofluorometry and immunoassays were used in pediatric MMA patients and compared to controls by age and sex. Elevated cEPC levels in peripheral blood and upregulation of angiogenic markers (ie, angiopoietin-2 and VEGF-A) in CSF were detected. This finding is likely related to deregulation of angiogenesis, as indicated by moderate collateral network development (Suzuki III-IV). The lack of significant modulation of neurofilament light in cerebrospinal fluid led us to rule out the presence of significant neuronal damage in children with MMA. Despite our limited cohort of pediatric patients, we found several unique cellular and molecular characteristics in their blood and CSF samples. Our results are supported by a more comprehensive and prospective study to identify predictive or prognostic circulating biomarkers and potential therapeutic targets for personalized care in pediatric MMA patients.