Sentence examples for myofibroblast phenotype is from inspiring English sources

Activation of resident fibroblasts leading to a myofibroblast phenotype is the principal feature that orchestrates this fibrotic process.

This suggests that the myofibroblast phenotype is not a permanent state but can be reversed by alterations in the matrix properties.

Age-related failure of TGF-β1- induced differentiation to the myofibroblast phenotype is associated with the inability to induce HAS2, a decrease in HA synthesis, and a lack of pericellular coat formation.

In contrast to this, studies culturing fibroblasts for prolonged periods on matrices of different mechanical properties suggest the conversion to a myofibroblast phenotype is a more "permanent" condition [ 65].

The conversion of hepatic stellate cells to a myofibroblast phenotype is a critical step in liver fibrosis and is part of the pathway to cirrhosis in chronic liver disease.

Similarly, fibroblast activation and differentiation to a contractile myofibroblast phenotype is important for wound closure and ECM deposition; however, if this tissue repair phase does not properly terminate, persistent myofibroblast activation can lead to excessive wound contraction and ECM deposition, again culminating in a fibrotic outcome (Gurtner et al., 2008; Serini and Gabbiana, 1996).

Bioactive environments regulating the myofibroblast phenotype were created by utilizing heparin glycosaminoglycan as a competitive inhibitor of HSPGs.

Factors that promote fibroblast differentiation and activation, such as growth factors and cytokines, are well studied; however, the mechanisms that contribute to the maintenance of the pro-fibrotic myofibroblast phenotype are less understood.

The molecular feature that defines the myofibroblast-like phenotype is reflected as an increased proportion of myofibroblast-like cells in the heterogeneous FLS population.

Transdifferentiation of hepatic stellate cells (HSCs) to a myofibroblast-like phenotype is the pivotal event in liver fibrosis.

The mechanism behind the evolution of PSCs from quiescent state to a cancer-associated myofibroblast-like phenotype is still not very clear.