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Analysis of the molecular mechanisms of vascular calcification from human clinical data.
EP37627
Poster Title: Analysis of the molecular mechanisms of vascular calcification from human clinical data.
Submitted on 01 Sep 2020
Author(s): А. Ibragimova, G. Mkrtchyan, A. Zubko, R. Komarov , Z. Malkandueva, A. Shindyapina.
Affiliations: MineGenics
This poster was presented at The 8th Annual Aging Research, Drug Discovery and Artificial Intelligence Forum 2020
Poster Views: 73
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Poster Information
Abstract: Introduction. 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.
Purpose. Investigation of the molecular mechanisms of vascular calcification from human clinical data.
Methods.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%).
Results.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.
Conclusions. 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.
Summary: To date, vascular calcification could be defined as a multifactorial process. To address this question we’ve collected surgically removed samples of the abdominal aorta and internal carotid artery.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. References: Report abuse »
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