Fibrosis occurs when the production of cross-linked collagen fibrils exceeds their degradation [1]. While there are multiple potential triggering stimuli and contributing factors to fibrotic progression, excessive accumulation of ECM components is still the end result. Several tissue types can be affected by fibrosis including skin, liver, heart, lung, intestine, and others. Lysyl oxidases (LOX) and transforming growth factor-beta1 (TGF-β1) contribute to fibrotic progression by increasing total collagen and collagen crosslinking in the ECM [1, 2]. This increased collagen crosslinking increases the elasticity and ultimate tensile strength of the affected tissue [3]. By measuring the tensile properties of TGF-β1 and LOX inhibitor-treated 3D in vitro self-assembled tissue ring models, we can show how the biomechanics of these ring tissues can be altered by the addition of different growth factors and drugs.
