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Genome-Wide Expression Analysis Suggests Hypoxia-Triggered Hyper-Coagulation Leading to Venous Thrombosis at High Altitude. | LitMetric

AI Article Synopsis

  • Venous thromboembolism (VTE) is a significant cardiovascular disease influenced by both genetic and environmental factors, with high altitude (HA) increasing risk but lacking clear molecular understanding.
  • This study investigated gene expression in deep vein thrombosis (DVT) patients from different altitudes and identified significant differences, revealing 378 genes at sea level and 875 genes at HA linked to DVT.
  • Analysis highlighted pathways related to haemostasis and platelet activation, with "response to hypoxia" emerging as key; specific hypoxia-responsive genes might help explain the development of DVT in high-altitude conditions.

Article Abstract

Venous thromboembolism (VTE), a multi-factorial disease, is the third most common cardiovascular disease. Established genetic and acquired risk factors are responsible for the onset of VTE. High altitude (HA) also poses as an additional risk factor, predisposing individuals to VTE; however, its molecular mechanism remains elusive. This study aimed to identify genes/pathways associated with the pathophysiology of deep vein thrombosis (DVT) at HA. Gene expression profiling of DVT patients, who developed the disease, either at sea level or at HA-DVT locations, resulted in differential expression of 378 and 875 genes, respectively. Gene expression profiles were subjected to bioinformatic analysis, followed by technical and biological validation of selected genes using quantitative reverse transcription-polymerase chain reaction. Both gene ontology and pathway analysis showed enrichment of genes involved in haemostasis and platelet activation in HA-DVT patients with the most relevant pathway being 'response to hypoxia'. Thus, given the environmental condition the differential expression of hypoxia-responsive genes (angiogenin, ribonuclease, RNase A family, 5; early growth response 1; lamin A; matrix metallopeptidase 14 [membrane-inserted]; neurofibromin 1; PDZ and LIM domain 1; procollagen-lysine 1, 2-oxoglutarate 5-dioxygenase 1; solute carrier family 6 [neurotransmitter transporter, serotonin], member 4; solute carrier family 9 [sodium/hydrogen exchanger], member 1; and TEK tyrosine kinase, endothelial) in HA-DVT could be a determining factor to understand the pathophysiology of DVT at HA.

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Source
http://dx.doi.org/10.1055/s-0038-1657770DOI Listing

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