Mechanotransduction is the process by which cells convert mechanical forces and deformations into biochemical signals, enabling them to adapt to their physical environment. This process is essential for cellular functions such as migration, proliferation, differentiation, and apoptosis, and is critical for organ development and homeostasis. Defects in mechanotransduction, often caused by mutations or misregulation of proteins, are implicated in various diseases, including muscular dystrophies, cardiomyopathies, cancer, and hearing loss. Mechanotransduction involves cellular processes that translate mechanical stimuli into biochemical signals. Research has identified several molecular players involved in this process, but many components remain incompletely defined. Sensory cells, such as hair cells in the inner ear, are often studied as models for mechanosensing. However, mechanotransduction is now recognized in a broader range of cells and tissues, including myocytes, endothelial cells, and vascular smooth muscle cells. Mechanotransduction is involved in various physiological processes, such as stem-cell differentiation, embryonic development, and tissue maintenance. For example, stem-cell differentiation can be influenced by the geometry and stiffness of the substrate, and intercellular physical interactions may be as important as concentration gradients of morphogenic factors in embryonic development. Defects in mechanotransduction can lead to various diseases. For instance, mutations in the dystrophin gene cause Duchenne muscular dystrophy by disrupting force transmission between the cytoskeleton and the extracellular matrix. Similarly, mutations in nuclear envelope proteins can lead to muscular dystrophies. In cancer, changes in ECM mechanics and cytoskeletal tension can promote malignant transformation, tumorigenesis, and metastasis. Mechanotransduction also plays a critical role in cardiovascular health. For example, laminar shear stress and circumferential vessel stretch exert an atheroprotective effect on endothelial cells. Disrupted fluid shear stress can lead to atherosclerosis. In the skeletal system, bone remodeling is influenced by mechanical stress, and in the kidney, urine flow regulates kidney morphogenesis. In the eye, disturbed mechanotransduction can contribute to glaucoma and axial myopia. In the case of Hutchinson-Gilford progeria syndrome, mutations in the LMNA gene lead to increased cellular sensitivity to mechanical strain, contributing to arteriosclerosis and other complications. Understanding mechanotransduction is crucial for developing therapeutic approaches to diseases. Research into mechanotransduction pathways could lead to new treatments for muscular dystrophies, cancer, and other conditions. Future studies should focus on the interplay of redundant or complementary mechanotransduction pathways and the development of targeted therapies for mechanotransduction diseases.Mechanotransduction is the process by which cells convert mechanical forces and deformations into biochemical signals, enabling them to adapt to their physical environment. This process is essential for cellular functions such as migration, proliferation, differentiation, and apoptosis, and is critical for organ development and homeostasis. Defects in mechanotransduction, often caused by mutations or misregulation of proteins, are implicated in various diseases, including muscular dystrophies, cardiomyopathies, cancer, and hearing loss. Mechanotransduction involves cellular processes that translate mechanical stimuli into biochemical signals. Research has identified several molecular players involved in this process, but many components remain incompletely defined. Sensory cells, such as hair cells in the inner ear, are often studied as models for mechanosensing. However, mechanotransduction is now recognized in a broader range of cells and tissues, including myocytes, endothelial cells, and vascular smooth muscle cells. Mechanotransduction is involved in various physiological processes, such as stem-cell differentiation, embryonic development, and tissue maintenance. For example, stem-cell differentiation can be influenced by the geometry and stiffness of the substrate, and intercellular physical interactions may be as important as concentration gradients of morphogenic factors in embryonic development. Defects in mechanotransduction can lead to various diseases. For instance, mutations in the dystrophin gene cause Duchenne muscular dystrophy by disrupting force transmission between the cytoskeleton and the extracellular matrix. Similarly, mutations in nuclear envelope proteins can lead to muscular dystrophies. In cancer, changes in ECM mechanics and cytoskeletal tension can promote malignant transformation, tumorigenesis, and metastasis. Mechanotransduction also plays a critical role in cardiovascular health. For example, laminar shear stress and circumferential vessel stretch exert an atheroprotective effect on endothelial cells. Disrupted fluid shear stress can lead to atherosclerosis. In the skeletal system, bone remodeling is influenced by mechanical stress, and in the kidney, urine flow regulates kidney morphogenesis. In the eye, disturbed mechanotransduction can contribute to glaucoma and axial myopia. In the case of Hutchinson-Gilford progeria syndrome, mutations in the LMNA gene lead to increased cellular sensitivity to mechanical strain, contributing to arteriosclerosis and other complications. Understanding mechanotransduction is crucial for developing therapeutic approaches to diseases. Research into mechanotransduction pathways could lead to new treatments for muscular dystrophies, cancer, and other conditions. Future studies should focus on the interplay of redundant or complementary mechanotransduction pathways and the development of targeted therapies for mechanotransduction diseases.