研究核心：細胞骨架與力學訊號傳導
我們實驗室的研究關注於細胞骨架與細胞力學的調控機制。細胞會接收來自外界的生化或物理訊號，並將這些訊號轉化為細胞內的指令，以調控細胞的形狀、附著與功能。我們發現細胞內Shp2分子能調控ROCK2，在細胞與基質接觸的焦點黏附處，幫助細胞感知外在的物理環境；而α-actinin-4分子則參與細胞骨架的穩定與黏附能力，尤其在腎臟的足細胞中扮演重要角色。
Core Research: Cytoskeletal Regulation and Mechanotransduction
Our lab focuses on how cells sense and respond to biochemical and physical cues from their environment. These signals are transduced into intracellular pathways that regulate cytoskeletal organization and cell mechanics. We have previously demonstrated that Shp2 regulates ROCK2 at focal adhesions, enhancing cell adhesion and cytoskeletal integrity through α-actinin-4-particularly in podocytes.

足細胞與腎臟疾病模型研究
足細胞是腎臟進行血液過濾最關鍵的細胞，具有特殊的足突結構形成過濾膜以防止蛋白質流失，因此，足細胞的受損往往會導致蛋白尿的發生，進而發展成慢性腎病。且因足細胞高度分化且不可再生的特性，其長期損傷或脫落，將導致慢性腎病的惡化，甚至進展至需洗腎的末期腎病。我們實驗室利用可誘導分化的足細胞株，並研發模擬過濾應力的體外實驗系統，嘗試探討其在受力狀態下的細胞骨架變化與基因表現改變；同時開發各種足細胞損傷模型，以了解不同腎毒性刺激下的足細胞損傷機制與藥物反應。希望透過這些研究，未來能提出新的策略，預防或延緩腎絲球病變的發生與惡化。
Podocytes and Kidney Disease Modeling
Podocytes are specialized glomerular epithelial cells forming the filtration barrier in the kidney. Their damage or detachment is a critical event in the progression of chronic kidney diseases. Our lab has developed an in vitro filtration-stress model to study cytoskeletal remodeling and transcriptional responses in differentiated podocytes. We also investigate various injury models to understand podocyte dysfunction and therapeutic responses.