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<p>Hypertension (HTN) is a mitochondrial and metabolic disease. However, cause-effect connections between mitochondrial dysfunction and HTN remains uncharted. we focused on mitochondria-related genes, identifying potential causal-genes-relevant blood pressure (BP) using mitochondria-related genome-wide Mendelian randomization (MR). Through the summary statistics from cis-expression quantitative trait loci (cis-eQTL) datasets (human blood and artery), mitochondrial transcription factor A (TFAM), and genome-wide association studies (GWAS) datasets of BP indices (systolic blood pressure [SBP], diastolic blood pressure [DBP], pulse pressure [PP], and mean arterial pressure [MAP]) and HTN. we conducted a MR analysis to explore the potential causal relationship between mitochondrial-related genes and the BP indices, HTN. Sensitivity analysis and Bayesian colocalization were employed to validate this causal relationship. In aorta, <i>HIBCH</i> expression was negatively associated with SBP; <i>OCIAD1</i> expression was positively associated with MAP. In tibial artery, <i>HIBCH</i> expression was negatively associated with SBP; <i>OCIAD1</i> expression was positively associated with SBP, PP, and MAP; <i>SLC25A37</i> was positively associated with MAP. In blood, <i>LACTB</i> expression was negatively associated with SBP, PP, and MAP; <i>OCIAD1</i> expression was negatively associated with SBP and PP; and <i>MTX1</i> expression was negatively associated with MAP. <i>HARS2</i> expression was positively associated with SBP and PP; <i>RAB24</i> and <i>PRELID1</i> expression was positively associated with DBP; and <i>NME6</i> expression was positively associated with SBP and DBP. In conclusion, the regulation of blood pressure correlates with mitochondria-related genes (<i>HIBCH, SLC25A37</i> and <i>OCIAD1</i> in artery; <i>LACTB</i>, <i>OCIAD1</i>, <i>MTX1</i>, <i>HARS2</i>, <i>RAB24</i>, <i>PRELID1</i> and <i>NME6</i> in blood). This study provides scientific evidence for specifically regulating BP phenotypes.</p>

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Identification of potential causal-genes-relevant blood pressure: a mitochondria-related genome-wide Mendelian randomization study

  • 期刊论文

  • 发表日期：

    2025年11月14日

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  • Hongrui Zhang,
  • Xiaoyang Li,
  • Yichen Liu,
  • Zhuoshuai Liang,
  • Ruofei Li,
  • Wenhui Gao,
  • Bo Wang,
  • Yuchen Zhang,
  • Yuyang Tian,
  • Xinmeng Hu,
  • Huizhen Jin,
  • Shuang Qiu,
  • Yong Li,
  • Yulu Gu,
  • Siyu Liu,
  • Yunkai Liu,
  • Yi Cheng,
  • Jikang Shi,
  • Yawen Liu

摘要

Hypertension (HTN) is a mitochondrial and metabolic disease. However, cause-effect connections between mitochondrial dysfunction and HTN remains uncharted. we focused on mitochondria-related genes, identifying potential causal-genes-relevant blood pressure (BP) using mitochondria-related genome-wide Mendelian randomization (MR). Through the summary statistics from cis-expression quantitative trait loci (cis-eQTL) datasets (human blood and artery), mitochondrial transcription factor A (TFAM), and genome-wide association studies (GWAS) datasets of BP indices (systolic blood pressure [SBP], diastolic blood pressure [DBP], pulse pressure [PP], and mean arterial pressure [MAP]) and HTN. we conducted a MR analysis to explore the potential causal relationship between mitochondrial-related genes and the BP indices, HTN. Sensitivity analysis and Bayesian colocalization were employed to validate this causal relationship. In aorta, HIBCH expression was negatively associated with SBP; OCIAD1 expression was positively associated with MAP. In tibial artery, HIBCH expression was negatively associated with SBP; OCIAD1 expression was positively associated with SBP, PP, and MAP; SLC25A37 was positively associated with MAP. In blood, LACTB expression was negatively associated with SBP, PP, and MAP; OCIAD1 expression was negatively associated with SBP and PP; and MTX1 expression was negatively associated with MAP. HARS2 expression was positively associated with SBP and PP; RAB24 and PRELID1 expression was positively associated with DBP; and NME6 expression was positively associated with SBP and DBP. In conclusion, the regulation of blood pressure correlates with mitochondria-related genes (HIBCH, SLC25A37 and OCIAD1 in artery; LACTB, OCIAD1, MTX1, HARS2, RAB24, PRELID1 and NME6 in blood). This study provides scientific evidence for specifically regulating BP phenotypes.