ArticleJournal of human hypertension2026
Identification of potential causal-genes-relevant blood pressure: a mitochondria-related genome-wide Mendelian randomization study.
Article in Journal of human hypertension, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Functional Diversity and Emerging Roles of Human NME/NDPK Group II Proteins.International journal of molecular sciences · 2026Review
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19 authors.
Funding
Abstract
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.
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