KCNK12 as a novel immune-related biomarker to reveal the crosstalk between COVID19 and stroke

Abstract

Background COVID-19, a respiratory disease that emerged in 2019, continues to pose a global threat to public health. Stroke has become the second leading cause of death worldwide, with respiratory infections among its serious complications. COVID-19 infection and mortality rates are notably higher among stroke patients than in the general population. However, the potential relationship between COVID-19 and stroke remains poorly understood. This article aims to elucidate the potential mechanisms underlying the association between these two diseases at the transcriptome level and to identify potentially useful drugs. Results KCNK12 was identified as an important stroke biomarker and showed significant differential expression in COVID-19 by intersecting multiple algorithms. Functional enrichment analysis revealed that KCNK12 primarily promotes neuroactive ligand-receptor interaction (p.adj < 0.001). Analysis of immune infiltration showed that neutrophils in the peripheral blood of stroke patients are the most affected by KCNK12. Moreover, there was a significant correlation between neuroactive ligand-receptor interaction and neutrophil infiltration (R = 0.65, p < 2.2e-16). The relationship between KCNK12 and neutrophil infiltration was further validated using single-cell data Conclusion We have identified KCNK12 as a potential target that may contribute to the susceptibility of stroke patients to COVID-19 infection. KCNK12 regulates neutrophil infiltration through neuroactive ligand-receptor interaction. This discovery not only sheds light on the underlying mechanisms of the relationship between stroke and COVID-19 but also provides predictions for transcription factors and potential drugs that can be used as therapeutic options.