ArticleSaudi journal of biological sciences2022
Identifying significant genes and functionally enriched pathways in familial hypercholesterolemia using integrated gene co-expression network analysis.
Article in Saudi journal of biological sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
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- A computational framework for identifying cytoskeletal genes associated with age-related diseases.Scientific reports · 2025Article
- Artificial Intelligence in Cardiology and Atherosclerosis in the Context of Precision Medicine: A Scoping Review.Applied bionics and biomechanics · 2024Article
- Identification of Plasma Exosomes hsa_circ_0001360 and hsa_circ_0000038 as Key Biomarkers of Coronary Heart Disease.Cardiology research and practice · 2024Article
- Network pharmacology based anti-diabetic attributes of bioactive compounds fromSaudi journal of biological sciences · 2023Article
- Rare variant burden analysis from exomes of three consanguineous families revealsFrontiers in medicine · 2023Article
- Exome Sequencing Identifies the Extremely RareFrontiers in pediatrics · 2022Article
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Familial hypercholesterolemia (FH) is a monogenic lipid disorder which promotes atherosclerosis and cardiovascular diseases. Owing to the lack of sufficient published information, this study aims to identify the potential genetic biomarkers for FH by studying the global gene expression profile of blood cells. The microarray expression data of FH patients and controls was analyzed by different computational biology methods like differential expression analysis, protein network mapping, hub gene identification, functional enrichment of biological pathways, and immune cell restriction analysis. Our results showed the dysregulated expression of 115 genes connected to lipid homeostasis, immune responses, cell adhesion molecules, canonical Wnt signaling, mucin type O-glycan biosynthesis pathways in FH patients. The findings from expanded protein interaction network construction with known FH genes and subsequent Gene Ontology (GO) annotations have also supported the above findings, in addition to identifying the involvement of dysregulated thyroid hormone and ErbB signaling pathways in FH patients. The genes like
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