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Abstract：
Fibrotic remodeling of the heart in response to injury contributes to heart failure, yet therapies to treat fibrosis remain elusive. Yes-associated protein (YAP) is activated in cardiac fibroblasts by myocardial infarction, and genetic inhibition of fibroblast YAP attenuates myocardial infarction-induced cardiac dysfunction and fibrosis. YAP promotes myofibroblast differentiation and associated extracellular matrix gene expression through engagement of TEA domain transcription factor 1 and subsequent de novo expression of myocardin-related transcription factor A. Thus, fibroblast YAP is a promising therapeutic target to prevent fibrotic remodeling and heart failure.
摘要：
心脏对损伤的纤维化重塑会导致心力衰竭，然而，治疗纤维化的疗法仍然难以捉摸。Yes相关蛋白（YAP）在心肌梗死的心肌成纤维细胞中被激活，和成纤维细胞YAP的遗传抑制可减轻心肌梗死引起的心脏功能障碍和纤维化。YAP通过参与TEA结构域转录因子1和随后的myocardin相关转录因子A的从头表达促进肌成纤维细胞分化和相关的细胞外基质基因表达。成纤维细胞YAP是预防纤维化重塑和心力衰竭的有希望的治疗靶标。
