The myofibroblast is a specialized fibroblast that expresses α-smooth muscle actin (α-SMA) and participates in wound contraction and fibrosis. The fibroblast to myofibroblast transition depends on chemical and mechanical signals. A fibroblast senses the changes in the environment (extracellular matrix (ECM)) and transduces these changes to the cytoskeleton and the nucleus, resulting in activation or inhibition of α-SMA transcription in a process called mechanosensing. A stiff matrix greatly facilitates the transition from fibroblast to myofibroblast, and although the aging heart is much stiffer than the young one, the aging fibroblast has difficulties in transitioning into the contractile phenotype. This suggests that the events occurring downstream of the matrix, such as activation or changes in expression levels of various proteins participating in mechanotransduction can negatively alter the ability of the aging fibroblast to become a myofibroblast. In this review, we will discuss in detail the changes in ECM, receptors (integrin or non-integrin), focal adhesions, cytoskeleton, and transcription factors involved in mechanosensing that occur with aging.

肌成纤维细胞是一种特殊的成纤维细胞，表达 α-平滑肌肌动蛋白 (α-SMA) 并参与伤口收缩和纤维化。成纤维细胞到肌成纤维细胞的转变取决于化学和机械信号。成纤维细胞感知环境（细胞外基质 (ECM)）的变化并将这些变化转导到细胞骨架和细胞核，从而在称为机械传感的过程中激活或抑制 α-SMA 转录。坚硬的基质极大地促进了从成纤维细胞到肌成纤维细胞的转变，虽然老化的心脏比年轻的心脏坚硬得多，但老化的成纤维细胞难以转变为收缩表型。这表明发生在矩阵下游的事件，例如，参与机械转导的各种蛋白质的激活或表达水平的变化会对老化的成纤维细胞成为肌成纤维细胞的能力产生负面影响。在这篇综述中，我们将详细讨论 ECM、受体（整联蛋白或非整联蛋白）、黏着斑、细胞骨架和参与机械感应的转录因子随衰老而发生的变化。