4.7 Article

Elevated Plasma Levels of C1qTNF1 Protein in Patients with Age-Related Macular Degeneration and Glucose Disturbances

Journal

JOURNAL OF CLINICAL MEDICINE
Volume 11, Issue 15, Pages -

Publisher

MDPI
DOI: 10.3390/jcm11154391

Keywords

AMD; age-related macular degeneration; C1qTNF; glucose disturbances

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Research has shown that inflammatory factors play an important role in the development of age-related macular degeneration (AMD) and glucose disturbances (GD), with C1qTNF1 identified as a key mediator in the integration of lipid metabolism and inflammatory responses.
In recent years, research has provided increasing evidence for the importance of inflammatory etiology in age-related macular degeneration (AMD) pathogenesis. This study assessed the profile of inflammatory cytokines in the serum of patients with AMD and coexisting glucose disturbances (GD). This prospective population-based cohort study addressed the determinants and occurrence of cardiovascular, neurological, ophthalmic, psychiatric, and endocrine diseases in residents of Bialystok, Poland. To make the group homogenous in terms of inflammatory markers, we analyzed only subjects with glucose disturbances (GD: diabetes or prediabetes). Four hundred fifty-six patients aged 50-80 were included. In the group of patients without macular degenerative changes, those with GD accounted for 71.7%, while among those with AMD, GD accounted for 89.45%. Increased serum levels of proinflammatory cytokines were observed in both AMD and GD groups. C1qTNF1 concentration was statistically significantly higher in the group of patients with AMD, with comparable levels of concentrations of other proinflammatory cytokines. C1qTNF1 may act as a key mediator in the integration of lipid metabolism and inflammatory responses in macrophages. Moreover, C1qTNF1 levels are increased after exposure to oxidized low-density lipoprotein (oxLDL), which plays a key role in atherosclerotic plaque formation and is also a major component of the drusen observed in AMD. C1qTNF1 may, therefore, prove to be a link between the accumulation of oxLDL and the induction of local inflammation in the development of AMD with concomitant GD.

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