Fibroid stiffness: a cellular modulator of progesterone receptor signaling

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Fibroids are characterized by the accumulation of extracellular matrix (ECM) and overexpression of collagens, giving these tumors their firm characteristics (1). This stiffness alters mechanotransduction, defined as a mechanism by which cells convert mechanical stimuli into biochemical signals. In addition, estrogen and progesterone through genomic and several nongenomic signaling pathways, including mitogen activated protein kinase, Rho-associated coiled-coil kinase (ROCK), phosphatidylinositol 3-kinase/protein kinase B, and Smads have a central role in regulating the growth of these tumors and the accumulation of ECM (2).