Fig. 1 Putative mechanisms of ECM stiffening and cellular contractile forces generated in response to increased microenvironment stiffness. Putative mechanisms.

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Presentation transcript:

Fig. 1 Putative mechanisms of ECM stiffening and cellular contractile forces generated in response to increased microenvironment stiffness. Putative mechanisms of ECM stiffening and cellular contractile forces generated in response to increased microenvironment stiffness. (A) Matrix cross-linking by lysyl oxidase (LOX), tissue transglutaminase (TG2), and advanced glycation end products (AGEs) in concert with increased matrix deposition are major contributors of pathological matrix stiffening. Inside-out and outside-in extracellular matrix (ECM) rigidity sensing is transmitted across cell adhesions composed of integrins and focal adhesion complexes. (B) Actomyosin cell contractility forces are increased in response to elevated matrix stiffness, and traction forces are exerted against the ECM. Cellular force is also propagated across the cell cytoplasm to the nucleus. (C) Stiffness-mediated traction forces transmitted across integrins cause a conformational change in the transforming growth factor β (TGFβ) latency complex to release TGFβ ligand and activate positive feedback cycles of ECM synthesis and stiffening. Solid blue arrows represent directionality of force transmission. Marsha C. Lampi and Cynthia A. Reinhart-King Sci Transl Med 2018;10:eaao0475 Copyright © 2018 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works