ArticleFrontiers in cardiovascular medicine2024
A Mendelian randomization study on the association between systemic inflammatory regulators and essential and secondary hypertension.
Article in Frontiers in cardiovascular medicine, 2024. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Causal correlation between inflammatory cytokines and hypertrophic scar based on two-sample Mendelian randomization.Journal, genetic engineering & biotechnology · 2025Article
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4 authors.
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Abstract
Background: Inflammation is an important driver of hypertension with numerous components, and there is a paucity of research on the specific inflammatory factors that induce hypertension; therefore, we wanted to investigate the relationship between specific inflammatory factors and hypertension. Purpose: A two-sample Mendelian randomization (MR) study was conducted to assess the causal relationship between systemic inflammatory regulators and hypertension (primary or secondary types). Method: a large-scale, published genome-wide association study (GWAS) meta-analysis encompassing 41 cytokines (involved 8,293 Finnish participants from three independent population cohorts: the Cardiovascular Risk in Young Finns Study (YFS), FINRISK1997, and FINRISK2002.)were utilized, a variety of analyses including MR-Egger, weighted median, simple mode and weighted mode were used as sensitive analyses, to corroborate the causal relationship between inflammatory regulators and hypertension. Additionally, we used MR-Egger intercept test and Mendelian Randomization Pleiotropy RE Sidual Sum and Outlier (MR-PRESSO global test) to further evaluate the presence of horizontal pleiotropy. Results: 3 inflammatory regulators were found related to secondary hypertension, TNFb was negatively associated with risk of secondary hypertension, with a OR of one SD increase in genetically predicted TNFb causing 16.6% (95% CI: 4.4%-27.1%) lower risk of secondary hypertension. Similar trend was also found in MIP1b (OR = 0.91; 95% CI 0.84-0.99, Conclusion: This study supports a negative correlation between TNFb, MIP1b, MIG and secondary hypertension.
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