Cardiac hypertrophy is a compensatory response to pathological stimuli, ultimately progresses to cardiomyopathy, heart failure, or sudden death. Although many signaling pathways have been reported to be involved in the hypertrophic process, it is still not fully clear about the underlying molecular mechanisms for cardiac hypertrophy. Hedgehog acyltransferase‐like (Hhatl), a sarcoplasmic reticulum‐resident protein, exhibits high expression in the heart and muscle. However, the biological role of Hhatl in the heart remains unknown. In this study, we first found that the expression level of Hhatl is markedly decreased in cardiac hypertrophy. We further studied the role of hhatla, homolog of Hhatl with the zebrafish model. The depletion of hhatla in zebrafish leads to cardiac defects, as well as an enhanced level of hypertrophic markers. Besides, we found that calcineurin signaling participates in hhatla depletion‐induced cardiac hypertrophy. Together, these results demonstrate a critical role for hhatla in cardiac hypertrophy.

中文翻译：

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斑马鱼 hhatla 与心脏肥大有关

心脏肥大是对病理刺激的代偿反应，最终发展为心肌病、心力衰竭或猝死。尽管已经报道了许多信号通路参与了肥大过程，但目前尚不完全清楚心脏肥大的潜在分子机制。Hedgehog 酰基转移酶样 (Hhatl) 是一种肌质网驻留蛋白，在心脏和肌肉中表现出高表达。然而，Hhatl 在心脏中的生物学作用仍然未知。在这项研究中，我们首先发现 Hhatl 的表达水平在心脏肥大中显着降低。我们进一步研究的作用hhatla，同源的Hhatl与斑马鱼模型。哈特拉的枯竭在斑马鱼中导致心脏缺陷，以及肥大标志物水平升高。此外，我们发现钙调神经磷酸酶信号参与hhatla耗竭诱导的心脏肥大。总之，这些结果证明了hhatla在心脏肥大中的关键作用。