| Autor: |
Sánchez-Gómez MC; Laboratory of Developmental Biology Research and Experimental Teratogenicity, Children's Hospital of Mexico Federico Gomez (HIMFG), CP 06720, Mexico City, Mexico.; School of Medicine, National Polytechnic Institute (IPN), Mexico City, Mexico., García-Mejía KA; Laboratory of Developmental Biology Research and Experimental Teratogenicity, Children's Hospital of Mexico Federico Gomez (HIMFG), CP 06720, Mexico City, Mexico., Pérez-Díaz Conti M; Department of Pathology, HIMFG, Mexico City, Mexico., Díaz-Rosas G; Laboratory of Developmental Biology Research and Experimental Teratogenicity, Children's Hospital of Mexico Federico Gomez (HIMFG), CP 06720, Mexico City, Mexico., Palma-Lara I; School of Medicine, National Polytechnic Institute (IPN), Mexico City, Mexico., Sánchez-Urbina R; Laboratory of Developmental Biology Research and Experimental Teratogenicity, Children's Hospital of Mexico Federico Gomez (HIMFG), CP 06720, Mexico City, Mexico., Klünder-Klünder M; Department of Community Health, HIMFG, Mexico City, Mexico., Botello-Flores JA; Laboratory of Developmental Biology Research and Experimental Teratogenicity, Children's Hospital of Mexico Federico Gomez (HIMFG), CP 06720, Mexico City, Mexico., Balderrábano-Saucedo NA; Laboratory of Cardiomyopathies and Arrhythmias, HIMFG, Mexico City, Mexico., Contreras-Ramos A; Laboratory of Developmental Biology Research and Experimental Teratogenicity, Children's Hospital of Mexico Federico Gomez (HIMFG), CP 06720, Mexico City, Mexico. acora_ramos@hotmail.com. |
| Abstrakt: |
Complex congenital heart disease (CHD) affects cardiac blood flow, generating a pressure overload in the compromised ventricles and provoking hypertrophy that over time will induce myocardial dysfunction and cause a potential risk of imminent death. Therefore, the early diagnosis of complex CHD is paramount during the first year of life, with surgical treatment of patients favoring survival. In the present study, we analyzed cardiac tissue and plasma of children with cardiac hypertrophy (CH) secondary to CHD for the expression of 11 miRNAs specific to CH in adults. The results were compared with the miRNA expression patterns in tissue and blood of healthy children. In this way, we determined that miRNAs 1, 18b, 21, 23b, 133a, 195, and 208b constitute the expression profile of the cardiac tissue of children with CHD. Meanwhile, miRNAs 21, 23a, 23b, and 24 can be considered specific biomarkers for the diagnosis of CH in infants with CHD. These results suggest that CH secondary to CHD in children differs in its mechanism from that described for adult hypertrophy, offering a new perspective to study the development of this pathology and to determine the potential of hypertrophic miRNAs to be biomarkers for early CH. |
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