The bladder is routinely subjected to mechanical stretch from filling cycles; however, abnormal bladder distention can result from pathological conditions such as bladder outlet obstruction. It has been suggested that abnormal mechanical environments in the bladder trigger cellular and molecular changes, such as smooth muscle cell hyperplasia or hypertrophy and alteration of the extracellular matrix (ECM). These cellular and ECM changes can, in turn, deteriorate the function of the bladder by decreasing the contractility and compliance of the tissue [1, 3, 5].

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