In silico analysis and verification of critical genes related to vascular calcification in multiple diseases

Identifying a functional molecular therapeutic target of vascular calcification (VC) that will not affect normal osteogenic differentiation is a challenge. To address this aim, we screened the differentially expressed genes (DEGs) in different VC conditions, including endothelial‐osteogenic transiti...

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Bibliographic Details
Published in:Cell biochemistry and function 2023-12, Vol.41 (8), p.1242-1251
Main Authors: Li, Shicheng, Ruan, Jiangwen, Yang, Zicong, Liu, Ling, Jiang, Tongmeng
Format: Article
Language:English
Subjects:
AKT protein
Animals
Arteriosclerosis
Atherosclerosis
Calcification
Calcification (ectopic)
Chemokines
Cholesterol
chronic kidney disease
Differentiation (biology)
endothelial‐osteogenic transition
Extracellular matrix
Genes
Hypertension
Hypertension - genetics
Immunohistochemistry
Kidney diseases
Kidneys
Kinases
Lipid metabolism
Mice
Osteogenesis
Phosphatidylinositol 3-Kinases
Polymerase chain reaction
Protein interaction
Proteins
Receptors
Renal Insufficiency, Chronic - genetics
Reverse transcription
Signal transduction
Therapeutic targets
vascular calcification
Vascular Calcification - genetics
Vascular Calcification - metabolism
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Summary:Identifying a functional molecular therapeutic target of vascular calcification (VC) that will not affect normal osteogenic differentiation is a challenge. To address this aim, we screened the differentially expressed genes (DEGs) in different VC conditions, including endothelial‐osteogenic transition (EOT) (GSE167962), chronic kidney disease (CKD), and atherosclerosis (AS) (GSE159832). KEGG pathways, protein–protein interactions, and hub genes were also analyzed. The intersecting DEGs among the EOT, CKD, and AS groups were verified by quantitative reverse transcription polymerase chain reaction and immunohistochemistry in a DOCA‐salt hypertension mouse model. The phosphoinositide 3‐kinase–protein kinase B signaling pathway, ECM‐receptor interaction, chemokine signaling pathway, and focal adhesion were enriched in EOT and AS‐induced VC. ECM‐receptor interaction, PPAR signaling pathway, apelin signaling pathway, AMPK signaling pathway, adipocytokine signaling pathway, and cholesterol metabolism were enriched in CKD and AS‐induced VC. C4b, Cebpa, Lyz2, and Spp1 were also upregulated in EOT, CKD, AS, and hypertension. This study identified promising molecular targets for VC therapy. Significance statement This research has pinpointed four crucial genes (C4b, Cebpa, Lyz2, and Spp1) linked to vascular calcification in various cardiovascular conditions such as chronic kidney disease, hypertension, atherosclerosis, and endothelial‐osteogenic transition.
ISSN:0263-6484
1099-0844
DOI:10.1002/cbf.3858