自体脂肪是最理想的软组织填充剂，但高达40%-60%的吸收率是限制其广泛临床应用的瓶颈。究其原因，关键在于缺乏对其存活及再生机制的深入了解。课题组前期研究发现，脂肪移植后移植物的主要"存活"模式是为以CD34阳性的脂肪前体细胞为核心、以新生血管为轴的小叶状的脂肪再生。进一步的研究发现，适当的炎症反应可以启动和诱导脂肪组织的新生。据此我们推测，炎症反应是启动脂肪再生的"门户"，通过对移植初期炎症反应的调控以诱导脂肪再生是决定脂肪移植转归的根本。本研究拟围绕炎症反应启动脂肪移植后脂肪再生的诱导及调控机制展开，采用组织移植、细胞生物、蛋白生化、基因检测及免疫组织化学技术，重点研究脂肪移植后炎症反应中炎症细胞诱导趋化、最佳炎症强度、炎症程度的人工调控这三大内容，阐明炎症反应与脂肪再生的密切相关性，并通过调节脂肪移植后早期炎症反应以启动移植后的脂肪再生来促进颗粒脂肪移植后的保存率。

Although autologous fat is the most ideal filling material, high absorption rate (40-60%) restrict its futher clinical application. This is because the survival and regenerative mechanism underlying adipose transplantation is not well known. Based on our previous findings, CD34 positive adipose precursor cell appears key to the process of neo-adipogenesis, in addition, upregulating the inflammation could significantly increase the neo-adipogenesis of normal adipose tissue. We hypothesize that the inflammation may play the "switch" role of neo-adipogenesis process after transplantion. The following research will focus on the mechanism of inflammation after transplantion，including the immune cells mobilization, the optimum intensity and regulation, by techniques concerning cytobiology, protein biochemistry in order to explore the mechanism of inflammation in neo-adipogenesis . This research is believed to be helpful to uncover the mechanism of inflammation of neo-adipogenesis, which will build a strong theoretical basis and provide stable experimental evidence for the improvement of retention of autologous adipose tissue transplantation.