心臟是推動全身血液循環的幫浦，而心肌細胞不止提供幫浦主要的動力來源，更具有主動回應環境訊號、減低環境機械性負荷、或者改變自身結構以適應環境的作用。目前已知神經體液性因素與機械性壓力在心臟重塑過程中扮演著重要角色，其中機械性壓力對心臟肥大的產生更是有著關鍵性的影響。由於病理性心肌肥大是許多心臟疾病的獨立危險因子，因此對於心臟科醫師而言，瞭解機械性壓力如何導致心臟肥大是相當重要的事。心肌細胞的力學訊號傳導意指心肌細胞偵測到機械性壓力的變化並做出反應；其過程可以被比喻為電腦指令的編碼與解碼過程。當心臟的負荷增加的時候（新的指令），這個訊號需要被適當的分子偵測、編碼（鍵盤），並經由第二級傳導物質（數位訊號）傳遞給下游分子 (CPU) 做出反應（解碼與執行指令），諸如收縮力的改變、離子平衡的改變、胞釋作用與基因的表現等。本篇文章主要目的就是探討心肌細胞力學訊號傳導的路狸與其臨床意義。

While the heart functions as a pump which pushes the blood through our circulation, the cardiomyocytes not only supply the major force of the pump, but also respond actively to various environmental signals to lower the mechanical loads or adapt themselves to the environmental requirements. It is known that neurohumoral factors and mechanical loads play important roles in the cardiac remodeling process, with the later having extremely great impact on cardiac hypertrophy. Since pathologic hypertrophy is an independent risk factor of many heart diseases, understanding how mechanical loads contribute to cardiac hypertrophy is necessary for cardiologists. Cardiac mechanotransduction indicates the process in which the cardiomyocytes sense the change of mechanical loads and react. It can be compared to the coding and decoding process of sending orders to the computer. When the loading of heart increases (new orders), the signals must be detected and coded by proper molecules (the keyboard), then transferred by second messengers (digital signals) to the downstream molecules (CPU) thus enables the cell to give proper reactions (decoding and performing orders), such as increasing of contractility, changing of the ion homeostasis, exocytosis and gene expression, etc. The aim of this article is to discuss the pathways involved in cardiac mechanotransduction and their clinical implications.