Figure 2 | Scientific Reports

Figure 2

From: Circulating antibodies against age-modified proteins in patients with coronary atherosclerosis

Figure 2

Molecular mechanisms, linking AGE-RAGE axis with systemic inflammation, and progression of COPD and CAD. CAD and COPD share a plethora of common risk factors, including lifestyle aspects and concomitant conditions, significantly exacerbating the course of both diseases. Chronic stimulation of the AGE-RAGE axis leads to overexpression of RAGE, completing the vicious circle that tunes metabolic and signaling pathways towards increased production of pro-fibrotic and pro-inflammatory factors. Anti-AGE-Abs might serve as an integral connector linking the risk factors of CAD and COPD with mechanisms triggering and supporting chronic inflammation, including AGE-RAGE-sRAGE triad. On the other hand by binding AGEs, anti-AGE-Abs might exert a protective function, similar to that of sRAGE. AGEs advanced glycation end-products, CABG coronary artery bypass grafting, CAD coronary artery disease, ECM extracellular matrix, IL interleukins, PKC-ζ protein kinase C isotype ζ, RAGE receptor to advanced glycation end-products, Rap1a small Ras-like GTPase, member of the Ras superfamily, SAA serum amyloid protein, TNF tumor necrosis factor.

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