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Insights into mechanisms of vascular calcification from human clinical data.
EP27550
Insights into mechanisms of vascular calcification from human clinical data.
Submitted on 23 Apr 2018

А. Ibragimova, G. Mkrtchyan, A. Zubko, R. Komarov , Z. Malkandueva, A. Shindyapina.
Peoples Friendship University of Russia (RUDN University)
This poster was presented at conference «Interventions to extend healthspan and lifespan» 2018
Poster Views: 147
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Poster Abstract
To date, vascular calcification could be defined as a multifactorial process that associates with age, atherosclerosis, chronic kidney diseases (CKD), diabetes, and chronic inflammatory disease.
The deposition of calcium phosphate crystals in the medial and intimal layers of the arteria increases the odds of stroke. Cell culture and animal studies provided insights into possible causes of vascular calcification. Among proposed mechanisms of vascular calcification in humans are deregulated calcium metabolism, chronic inflammation, smooth muscle cells reprogramming, and abnormal phosphate metabolism. However, the precise mechanism of vascular calcification in humans remain largely unknown.
To address this question we’ve collected surgically removed samples of the abdominal aorta and internal carotid artery. Presence of calcium deposits was histologically detected in half of the patients that confirming the high prevalence of calcification among diverse cardiovascular pathologies. Based on calcified area samples were classified as free of calcification, moderate (<10% of vessel area) and extremely calcified (>10%). Gene expression analysis of 16 artery samples from 3 females and 13 males (mean age 65, interval 44-79) was performed by microarrays. The principal component analysis clearly separated samples with extreme calcification from control samples, while vessel type, sex, age, and body mass index (BMI) had no effect on clusterization. Interestingly, neither BMI, cholesterol, HDL, LDL, or VLDL showed any correlation with calcification status, while sedimentation rate of erythrocyte was strongly positively associated with the severity of calcification (4.7±3.8 vs 18±3, p < 0.01). Thus, inflammation may contribute to calcification development more than aberrant fat metabolism. Enrichment analysis among genes that positively correlates with calcification status revealed the possible involvement of ubiquitin-related pathways in calcification development. Surprisingly, none of the previously proposed regulators of vascular calcification among osteogenesis pathways had altered expression.
This pilot study of 16 patients revealed the possible role of inflammation and ubiquitin-related pathways in the development of vascular calcification in humans while alteration of osteogenesis pathways seems like has no impact.
The publication was prepared with the support of the “ RUDN University Program 5-100”.

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