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A recent Mendelian randomization (MR) did not support an effect of the lead interleukin-6 receptor (IL-6 R) variant on risk of pulmonary arterial hypertension (PAH). Thus, we used two sets of genetic instrumental variants (IVs) and publicly available PAH genome-wide association studies (GWAS) to reassess the genetic causal link between IL-6 signaling and PAH. Six independent IL-6 signaling and 34 independent soluble IL-6 receptor (sIL-6 R) genetic IVs from recent MR reports and PAH GWAS including 162,962 European individuals were used to perform this two-sample MR study. We found that as IL-6 signaling genetically increased, the risk of PAH reduced using IVW (odds ratio [OR] = 0.023, 95% confidence interval [CI]: 0.0013–0.393;  p  = .0093) and weighted median (OR = 0.033, 95% CI: 0.0024–0.467;  p  = .0116). Otherwise, as sIL-6 R genetically increased, the risk of PAH increased using IVW (OR = 1.34, 95% CI: 1.16–1.56;  p  = .0001), weighted median (OR = 1.36, 95% CI: 1.10–1.68;  p  = .005), MR-Egger (OR = 1.43, 95% CI: 1.05–1.94;  p  = .03), and weighted mode (OR = 1.35, 95% CI for OR: 1.12–1.63;  p  = .0035). Our analysis suggested the causal link between genetically increased sIL-6 R and increased risk of PAH and between genetically increased IL-6 signaling and reduced risk of PAH. Thus, higher sIL-6 R levels may be a risk factor for patients with PAH, whereas higher IL-6 signaling may be a protective factor for patients with PAH.

Mendelian randomization study on causal association of IL-6 signaling with pulmonary arterial hypertension