No genetic causal association between iron status and pulmonary artery hypertension: Insights from a two‐sample Mendelian randomization

Author:

Liu Peng‐Cheng1ORCID,Lv Meng‐Na2ORCID,Rong Yan‐Yan3ORCID,Yu Shu‐Jiao1ORCID,Wu Rui1ORCID

Affiliation:

1. Department of Rheumatology, The First Affiliated Hospital, Jiangxi Medical College Nanchang University Nanchang China

2. The First Clinical Medical College of Nanchang University Nanchang China

3. Department of Hematology, The First Affiliated Hospital, Jiangxi Medical College Nanchang University Nanchang China

Abstract

AbstractTo explore the genetic causal association between pulmonary artery hypertension (PAH) and iron status through Mendelian randomization (MR), we conducted MR analysis using publicly available genome‐wide association study (GWAS) summary data. Five indicators related to iron status (serum iron, ferritin, total iron binding capacity (TIBC), soluble transferrin receptor (sTfR), and transferrin saturation) served as exposures, while PAH was the outcome. The genetic causal association between these iron status indicators and PAH was assessed using the inverse variance weighted (IVW) method. Cochran's Q statistic was employed to evaluate heterogeneity. We assessed pleiotropy using MR‐Egger regression and MR‐Presso test. Additionally, we validated our results using the Weighted median, Simple mode, and Weighted mode methods. Based on the IVW method, we found no causal association between iron status (serum iron, ferritin, TIBC, sTfR, and transferrin saturation) and PAH (pβ > 0.05). The Weighted median, Simple mode, and Weighted mode methods showed no potential genetic causal association (pβ > 0.05 in the three analyses). Additionally, no heterogeneity or horizontal pleiotropy was detected in any of the analyses. Our results show that there are no genetic causal association between iron status and PAH.

Funder

National Natural Science Foundation of China

Publisher

Wiley

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