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<p>SUMOylation and potassium channels have been implicated in pulmonary arterial hypertension (PAH). This study was designed to identify key hub genes associated with these pathways and investigate their mechanistic roles.&#xa0;We integrated data from the GSE131793, GSE113439, and GSE228644 datasets to obtain candidate genes associated with SUMOylation and potassium channels. Machine learning algorithms and expression verification were employed to identify the hub genes. Subsequently, we constructed regulatory networks and performed single-cell analysis to annotate distinct cell populations. Cell communication and pseudotime analyses were then analyzed. Quantitative polymerase chain reaction (qPCR) validation was conducted on samples from 5 idiopathic PAH (IPAH) patients and 5 controls.&#xa0;An initial list of 26 candidate genes was obtained, which was then narrowed by our screening strategy to ATP1B1, CD151, HP, IL18RAP, and VSTM1. Of these, ATP1B1 and HP showed consistent expression trends and were defined as hub genes. Both genes were positively correlated with the Fc gamma R-mediated phagocytosis and Lysosome pathways. In the single-cell analysis, multiple cell types, including fibroblasts, monocytes/macrophages, and T cells, were annotated. Notably, epithelial cells interacted exclusively with fibroblasts in the control group. Pseudotime analysis suggested ATP1B1 and HP are involved in transitioning epithelial cells from normal to diseased states. qPCR confirmed significantly elevated expression of ATP1B1 and HP in PAH patients (<i>p</i> &lt; 0.05).&#xa0;ATP1B1 and HP were identified as key hub genes in PAH, potentially influencing immune and inflammatory pathways during PAH development.</p> Graphic Abstract <p></p>

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Identification of Key Genes Related to SUMOylation and Potassium Channels and Their Mechanism of Influence on Pulmonary Arterial Hypertension

  • 期刊论文

  • 发表日期：

    2026年4月30日

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  • Lingyun Gao,
  • Wei Huang,
  • Qianqian Wang,
  • Sen Lei

摘要

SUMOylation and potassium channels have been implicated in pulmonary arterial hypertension (PAH). This study was designed to identify key hub genes associated with these pathways and investigate their mechanistic roles. We integrated data from the GSE131793, GSE113439, and GSE228644 datasets to obtain candidate genes associated with SUMOylation and potassium channels. Machine learning algorithms and expression verification were employed to identify the hub genes. Subsequently, we constructed regulatory networks and performed single-cell analysis to annotate distinct cell populations. Cell communication and pseudotime analyses were then analyzed. Quantitative polymerase chain reaction (qPCR) validation was conducted on samples from 5 idiopathic PAH (IPAH) patients and 5 controls. An initial list of 26 candidate genes was obtained, which was then narrowed by our screening strategy to ATP1B1, CD151, HP, IL18RAP, and VSTM1. Of these, ATP1B1 and HP showed consistent expression trends and were defined as hub genes. Both genes were positively correlated with the Fc gamma R-mediated phagocytosis and Lysosome pathways. In the single-cell analysis, multiple cell types, including fibroblasts, monocytes/macrophages, and T cells, were annotated. Notably, epithelial cells interacted exclusively with fibroblasts in the control group. Pseudotime analysis suggested ATP1B1 and HP are involved in transitioning epithelial cells from normal to diseased states. qPCR confirmed significantly elevated expression of ATP1B1 and HP in PAH patients (p < 0.05). ATP1B1 and HP were identified as key hub genes in PAH, potentially influencing immune and inflammatory pathways during PAH development.

Graphic Abstract