Mechanobiology of YAP and TAZ in physiology and disease

Mechanobiology of YAP and TAZ in physiology and disease

2017 December | Tito Panciera, Luca Azzolin, Michelangelo Cordenonsi, Stefano Piccolo
YAP and TAZ are key mechanotransducers that sense and transduce mechanical cues into cellular responses, regulating gene expression and influencing physiological and pathological processes. These proteins respond to various mechanical signals, including ECM rigidity, cell shape, and shear stress, and are critical for stem cell behavior, tissue regeneration, and the onset of diseases such as atherosclerosis, fibrosis, and cancer. YAP and TAZ are regulated by the cytoskeleton, particularly through F-actin organization, and their activity is influenced by mechanical forces that affect cell shape, ECM stiffness, and cell adhesion. They are also involved in tissue homeostasis, wound healing, and organ development, with their activity being modulated by signaling pathways such as Hippo, Rho, and FAK. YAP and TAZ mechanotransduction is essential for cell proliferation, differentiation, and survival, and their dysregulation is linked to disease progression. In cancer, YAP and TAZ are activated by the tumor microenvironment, promoting tumor growth, metastasis, and resistance to therapy. Targeting YAP and TAZ mechanotransduction offers potential therapeutic strategies for diseases involving abnormal mechanical signaling. The study of YAP and TAZ mechanotransduction provides insights into the molecular mechanisms underlying tissue mechanics and disease pathogenesis.YAP and TAZ are key mechanotransducers that sense and transduce mechanical cues into cellular responses, regulating gene expression and influencing physiological and pathological processes. These proteins respond to various mechanical signals, including ECM rigidity, cell shape, and shear stress, and are critical for stem cell behavior, tissue regeneration, and the onset of diseases such as atherosclerosis, fibrosis, and cancer. YAP and TAZ are regulated by the cytoskeleton, particularly through F-actin organization, and their activity is influenced by mechanical forces that affect cell shape, ECM stiffness, and cell adhesion. They are also involved in tissue homeostasis, wound healing, and organ development, with their activity being modulated by signaling pathways such as Hippo, Rho, and FAK. YAP and TAZ mechanotransduction is essential for cell proliferation, differentiation, and survival, and their dysregulation is linked to disease progression. In cancer, YAP and TAZ are activated by the tumor microenvironment, promoting tumor growth, metastasis, and resistance to therapy. Targeting YAP and TAZ mechanotransduction offers potential therapeutic strategies for diseases involving abnormal mechanical signaling. The study of YAP and TAZ mechanotransduction provides insights into the molecular mechanisms underlying tissue mechanics and disease pathogenesis.
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