Since the discovery of oxidized low-density lipoprotein (Ox-LDL), over 6,000 articles have appeared on the topic with over 4000 articles appearing during the past decade. Numerous studies have documented that oxidized lipids as well as products derived from their decomposition have deleterious biological properties. A plethora of in vitro and animal studies, as well as human epidemiological studies, have supported the notion that oxidative processes and the formation of Ox-LDL might contribute to atherosclerosis. Ox-LDL is taken up by macrophages via scavenger receptors, such as SR-A1, SR-A2, and LOX-1. Oxidized LDL mediates many proatherogenic and proinflammatory pathways. Minimally modified LDL also induces proinflammatory effects in macrophages, which are mediated through toll-like receptor-4, including cytoskeletal rearrangements and macropinocytosis, generation of reactive oxygen species, survival of foam cells, and expression of inflammatory genes. We are interested in articles that explore aspects of oxidized LDL molecules in inflammation. Potential topics include, but are not limited to:

• The role of oxidized LDL in chronic inflammation
• The incidence of coronary artery disease in patients with inflammatory disorders
• Relationship between atherosclerosis and chronic infection
• Specific effects of oxidized LDL on macrophages in inflammation
• Mouse models of oxidized LDL in inflammation
• Oxidized LDL and ischemia-reperfusion injury
• Involvement of oxidized LDL in autophagy and inflammasome activation
• Intracellular signaling induced by oxidized LDL
• Relationship between oxidized LDL and cellular senescence in inflammation
• Involvement of oxidized LDL in apoptosis
• Effects of oxidized LDL on gut microbiota

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