BackgroundEpilepsy is a disorder that can manifest as abnormalities in neurological or physical function. Stress cardiomyopathy is closely associated with neurological stimulation. However, the mechanisms underlying the interrelationship between epilepsy and stress cardiomyopathy are unclear. This paper aims to explore the genetic features and potential molecular mechanisms shared in epilepsy and stress cardiomyopathy.MethodsBy analyzing the epilepsy dataset and stress cardiomyopathy dataset separately, the intersection of the two disease co-expressed differential genes is obtained, the co-expressed differential genes reveal the biological functions, the network is constructed, and the core modules are identified to reveal the interaction mechanism, the co-expressed genes with diagnostic validity are screened by machine learning algorithms, and the co-expressed genes are validated in parallel on the epilepsy single-cell data and the stress cardiomyopathy rat model.ResultsEpilepsy causes stress cardiomyopathy, and its key pathways are Complement and coagulation cascades, HIF-1 signaling pathway, its key co-expressed genes include SPOCK2, CTSZ, HLA-DMB, ALDOA, SFRP1, ERBB3. The key immune cell subpopulations localized by single-cell data are the T_cells subgroup, Microglia subgroup, Macrophage subgroup, Astrocyte subgroup, and Oligodendrocytes subgroup.ConclusionWe believe epilepsy causing stress cardiomyopathy results from a multi-gene, multi-pathway combination. We identified the core co-expressed genes (SPOCK2, CTSZ, HLA-DMB, ALDOA, SFRP1, ERBB3) and the pathways that function in them (Complement and coagulation cascades, HIF-1 signaling pathway, JAK-STAT signaling pathway), and finally localized their key cellular subgroups (T_cells subgroup, Microglia subgroup, Macrophage subgroup, Astrocyte subgroup, and Oligodendrocytes subgroup). Also, combining cell subpopulations with hypercoagulability as well as sympathetic excitation further narrowed the cell subpopulations of related functions.
Sleep is essential to the normal psychological and physiological activities of the human body. Increasing evidenceindicates that sleep deprivation is associated with the occurrence, development, and poor treatment effects of variousarrhythmias. Sleep deprivation affects not only the peripheral nervous system but also the central nervous system,which regulates the occurrence of arrhythmias. In addition, sleep deprivation is associated with apoptotic pathways,mitochondrial energy metabolism disorders, and immune system dysfunction. Although studies increasingly suggestthat pathological sleep patterns are associated with various atrial and ventricular arrhythmias, further research is neededto identify specific mechanisms and recommend therapeutic interventions. This review summarizes the findings ofsleep deprivation in animal experiments and clinical studies, current challenges, and future research directions in thefield of arrhythmias.
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