FIG. 4.

Metabolic stress enhances monocyte adhesion and recruitment via S-glutathionylation of mitogen-activated protein kinase phosphatase 1 (MKP-1). Metabolic stress induces H₂O₂-mediated S-glutathionylation of MKP-1, resulting in MKP-1 inactivation and degradation. As a result, hyperactivation (increased phosphorylation) of both ERK and p38MAPK signaling occurs, which leads to enhanced monocyte adhesion and chemotaxis, respectively. These metabolic stress-induced changes in protein signaling and monocyte migration can be reversed by increased Grx1 expression. To see this illustration in color, the reader is referred to the web version of this article at www.liebertpub.com/ars