GLRX (glutaredoxin) is a 12 kDa cytosolic enzyme localized to chromosome 5 1 that catalyzes glutathione-dependent disulfide oxidoreduction reactions, primarily removing S-glutathionylation modifications from proteins 2. This deglutathionylation activity maintains protein thiols in a reduced state and transduces redox signals into biological responses 2. Mechanistically, GLRX regulates vascular and inflammatory processes by modulating NF-κB signaling and protein S-glutathionylation status 3. It controls the Wnt5a/sFlt-1 pathway, which regulates neovascularization and endothelial cell function 3. GLRX also influences apoptosis and cell proliferation through effects on pro-apoptotic proteins and redox-sensitive signaling cascades 4. Diseases linked to GLRX dysregulation include thoracic aortic aneurysm, where GLRX is differentially expressed in vascular smooth muscle cells 5, Alzheimer's disease with circadian rhythm disruption 6, myocardial infarction 7, lymphangioleiomyomatosis 4, and idiopathic pulmonary fibrosis, where GLRX modulates collagen S-glutathionylation and fibroblast activation 8. Clinically, GLRX represents a potential therapeutic target: Glrx overexpression impairs post-ischemic neovascularization 3, while Glrx deletion protects against certain pathologies 2. Modulating GLRX activity could provide novel treatment strategies for cardiovascular, neurodegenerative, and fibrotic diseases.