Sentence examples for matrix reviewed in from inspiring English sources

ROS and RNS have been implicated in a variety of cell signaling pathways, including growth factor signaling [6], [7], inflammation [33], engagement of integrins [34], [35], and adhesion to extracellular matrix (reviewed in [36]).

Mammalian mir-29 has been previously implicated in regulating cellular proliferation, differentiation, apoptosis, and the extracellular matrix (reviewed in Boominathan 2010; Kriegel et al. 2012).

Inhibitors of integrin function include function-blocking monoclonal antibodies, peptide antagonists and small molecule peptide mimetics matrix (reviewed in Hynes, 1992; Cheresh, 1993).

TGF-β is initially produced in its latent form [ 31, 32], that is, covalently linked with the latency-associated proteins and attached to LTBPs, which are cross-linked to the extracellular matrix (reviewed in [ 17]).

This is consistent with studies showing that after cartilage microtrauma, there is an increase in inflammatory mediators, including inflammatory cytokines, in synovial fluid, which stimulate catabolic enzymes that breakdown articular cartilage matrix (reviewed in [ 120]).

The glycosaminoglycan (GAG, a proteoglycan side chain) content decreases and catabolic matrix metalloproteinase (MMP) activity and denatured collagen content increases - the latter creating a more rigid IVD matrix reviewed in [ 2, 5, 6].

Activation of MMPs results in the degradation of collagens in the extracellular matrix (reviewed by Coussens and Werb 2002).

S100A4 promotes angiogenesis and extracellular matrix degradation through its upregulation of specific matrix metalloproteases (reviewed in Helfman et al, 2005) and high levels of S100A4 expression are associated with metastatic progression in a wide range of cancers including medulloblastoma (Hernan et al, 2003).

ROS and RNS damage cellular elements in cartilage directly and damage components of the extracellular matrix either directly or indirectly by upregulating mediators of matrix degradation (reviewed in [ 2, 26]).

Expression of the mir-29 miRNAs are regulated by both c-Myc and NF-κB and have been shown to regulate genes involved in apoptosis, cell proliferation, differentiation, and extracellular matrix components (reviewed in Kriegel et al. 2012).

The binding site of a CII-binding antibody is often the site for binding of matrix proteins (reviewed in [ 10]), which could explain why the epitope specificity of the antibodies is important for their pathogenicity.