应激性心肌病（SIC）引起暂时性心功能障碍，钙转运紊乱是SIC的发病机制之一，但其恢复机制目前仍不清楚。前期发现，肝细胞瘤衍生生长因子（HDGF）在SIC恢复期表达上调。抑制HDGF的表达降低钙转运及心肌功能的恢复。抑制因子-1（I-1）在恢复期表达增加，且HDGF可促进I-1的表达，提高心肌功能。结果提示HDGF在SIC恢复期钙转运中起重要作用。目前未见关于HDGF在SIC中的研究报道。据此，我们提出假说：HDGF可通过调控I-1的表达，改善心肌细胞钙转运，促进SIC心肌功能的恢复。本研究运用过量异丙肾上腺素诱导SIC模型，拟从分子、细胞以及动物水平等多层次明确HDGF在SIC心肌功能恢复中发挥的作用；探究HDGF通过调控I-1的表达影响心肌钙转运及心肌功能恢复的分子机制。本项目将从心功能恢复期HDGF的改变这一新视角探讨SIC心肌功能的恢复机制，为治疗SIC和促进心功能恢复提供新思路。

Stress-induced cardiomyopathy results in temporary cardiac dysfunction, in which the disorder of calcium handling is one of the mechanisms. So far, the mechanism of SIC recovery remains unclear. Previously, we found that Hepatoma-derived growth factor(HDGF) was up-regulated during recovery of SIC and inhibition of HDGF reduced cardiac function, calcium cycling and contractility of myocytes. Expression of Inhibitor-1(I-1) was increased in the recovery phase, and exogenous HDGF induced I-1 expression, promoted calcium cycling and recovery of cardiac function. These results suggested the important role of HDGF in calcium handling during recovery of SIC. HDGF has not been reported to be functioning in SIC currently. Therefore, we hypothesized that: HDGF improves myocytes calcium handling performance and ameliorate cardiac function through I-1 up-regulation. This project will apply SIC mouse model induced by over-dose injection of isopreterenol to identify the role of HDGF in cardiac function recovery of SIC; explore the molecular mechanism in I-1-dependent regulation of calcium cycling and cardiac function recovery induced by HDGF. This project will novelly focus on function of HDGF in recovery phase of SIC to study the mechanism of SIC, and it may provide new strategy for SIC treatment and promotion of cardiac function.