S-glutathionylation in monocyte and macrophage (dys)function.

Area of Science:

• Cardiovascular Biology
• Cellular Redox Biology
• Immunology

Background:

• Atherosclerosis is a chronic inflammatory disease driven by monocytes and macrophages.
• Oxidative stress, an imbalance between reactive oxygen species (ROS) and antioxidants, is implicated in atherosclerosis.
• ROS target protein thiols, altering cellular functions.

Purpose of the Study:

• To review the role of thiol oxidative stress and protein-S-glutathionylation in monocyte and macrophage dysfunction.
• To explore the link between oxidative stress in metabolic disorders and chronic inflammatory diseases like atherosclerosis.

Main Methods:

• Literature review focusing on thiol oxidation, S-glutathionylation, and immune cell function.
• Analysis of the mechanistic link between metabolic disorders, oxidative stress, and atherosclerosis.

Main Results:

• Protein-S-glutathionylation, initially viewed as a marker of oxidative stress, is now recognized as a critical redox signaling mechanism.
• Dysregulated S-glutathionylation contributes to various disease processes.
• Thiol oxidative stress and S-glutathionylation impair monocyte and macrophage function.

Conclusions:

• Protein-S-glutathionylation and thiol oxidative stress are key players in monocyte and macrophage dysfunction.
• These processes mechanistically link metabolic disorders-associated oxidative stress to chronic inflammatory diseases, including atherosclerosis.