The Myofibroblast

Abstract

The crucial role played by the myofibroblast in wound healing and pathological organ remodeling is well established; the general mechanisms of extracellular matrix synthesis and of tension production by this cell have been amply clarified. This review discusses the pattern of myofibroblast accumulation and fibrosis evolution during lung and liver fibrosis as well as during atheromatous plaque formation. Special attention is paid to the specific features characterizing each of these processes, including the spectrum of different myofibroblast precursors and the distinct pathways involved in the formation of differentiated myofibroblasts in each lesion. Thus, whereas in lung fibrosis it seems that most myofibroblasts derive from resident fibroblasts, hepatic stellate cells are the main contributor for liver fibrosis and media smooth muscle cells are the main contributor for the atheromatous plaque. A better knowledge of the molecular mechanisms conducive to the appearance of differentiated myofibroblasts in each pathological situation will be useful for the understanding of fibrosis development in different organs and for the planning of strategies aiming at their prevention and therapy.

MiR-21 Mediates Fibrogenic Activation Of Pulmonary Fibroblasts And Lung Fibrosis

“…TGF-1 induces fibroblast differentiation into more fibrogenic myofibroblasts (Hinz et al, 2007). We showed above that enhanced miR-21 expression in bleomycin-treated mice was primarily localized to -SMA-expressing myofibroblasts.…”

“…Pulmonary fibroblasts are primary effectors of lung fibrotic diseases (Hinz et al, 2007). TGF-1 induces fibroblast differentiation into more fibrogenic myofibroblasts (Hinz et al, 2007).…”

Krüppel-like Factor 5 Shows Proliferation-specific Roles in Vascular Remodeling, Direct Stimulation of Cell Growth, and Inhibition of Apoptosis

“…Cell cycle analysis showed markedly increased S-phase bulging after KLF5 transfection both in myofibroblasts and in VSMCs, which are the two major cellular components of vascular remodeling (Fig. 2B) (24).…”

Decorin Interacts with Connective Tissue Growth Factor (CTGF)/CCN2 by LRR12 Inhibiting Its Biological Activity

“…This complex biological process includes an inflammatory response and the activation of fibroblasts to myofibroblasts that have a highly contractile phenotype and are the principal source of connective tissue and extracellular matrix (ECM) 3 proteins, such as collagen and fibronectin (4). The development of fibrosis is the consequence of the action of growth factors and cytokines that are overexpressed in fibrotic tissues.…”