Consulta: creatorFacets:"Huang,Z."
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Data/hora: 10/06/2024 17:36:06

Overexpression of myeloid differentiation protein 88 in mice induces mild cardiac dysfunction, but no deficit in heart morphology
Provedor de dados: 56
Autores: Chen,W.; Huang,Z.; Jiang,X.; Li,C.; Gao,X.
Cardiac remodeling involves changes in heart shape, size, structure, and function after injury to the myocardium. The proinflammatory adaptor protein myeloid differentiation protein 88 (MyD88) contributes to cardiac remodeling. To investigate whether excessive MyD88 levels initiate spontaneous cardiac remodeling at the whole-organism level, we generated a transgenic MyD88 mouse model with a cardiac-specific promoter. MyD88 mice (male, 20-30 g, n=∼80) were born at the expected Mendelian ratio and demonstrated similar morphology of the heart and cardiomyocytes with that of wild-type controls. Although heart weight was unaffected, cardiac contractility of MyD88 hearts was mildly reduced, as shown by echocardiographic examination, compared with wild-type...
Tipo: Info:eu-repo/semantics/article
Palavras-chave: Cardiac dysfunction; Cardiac remodeling; Transgenic mice; Myeloid differentiation protein 88.
Ano: 2016
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2016000100605