Introduction: Cerebral Venous Sinus Thrombosis (CVST) is a disease with a low incidence rate but is prone to progression and Early Deterioration of Parenchymal Lesions (EDPL), leading to severe neurological impairment. Exploring the potential molecular mechanisms and key genes of EDPL to achieve early clinical intervention and treatment is of vital importance. This study aims to investigate the potential molecular mechanisms and key genes of EDPL in CVST. Methods: The CVST patients were prospectively recruited, and their peripheral venous blood was collected. The gene expression matrices of three EDPL patients and three non-EDPL patients were obtained by transcriptome sequencing technology, differentially expressed genes were analyzed, a competing endogenous RNA (ceRNA) network for lncRNA-miRNA-mRNA was constructed, and the target genes of the ceRNA network were subjected to GO and KEGG analyses. The Hub genes of differentially expressed mRNAs (DEmRNAs) were screened using Cytoscape. Subsequently, the key genes were obtained by intersecting the Hub genes with the target genes. Results: In the present study, 172 differentially expressed lncRNAs (DElncRNAs, 145 upregulated and 27 down-regulated) and 107 DEmRNAs (53 up-regulated and 54 down-regulated) were obtained between the EDPL group and the non-EDPL group. We constructed a ceRNA network of EDPL containing 75 DElncRNAs, 34 miRNAs, and 46 DEmRNAs, and explored the functional enrichment of the target genes in the ceRNA network. It was shown that the target genes were mainly concentrated in the focal adhesion and the ECM-receptor interaction. Subsequently, the target genes of the ceRNA network were intersected with the Hub genes, and four key genes (RELN, CAV1, CCNB1, NME1-NME2) were screened. Discussion: This study constructed the ceRNA regulatory network of EDPL to analyze the potential mechanisms and screen key genes, but there are still certain limitations, such as a small sample size and a lack of in vivo and in vitro experimental verification. Large-scale, multicenter, and prospective studies are needed to further verify these results. Conclusion: It was shown that focal adhesion and ECM-receptor interaction may be involved in the mechanisms of EDPL, and RELN, CAV1, CCNB1, and NME1-NME2 may be promising intervention targets for EDPL.
Cen et al. (Mon,) studied this question.