Multi-biobank summary data Mendelian randomisation does not support a causal effect of IL-6 signalling on risk of pulmonary arterial hypertension

Interleukin-6 (IL-6) has been linked with the pathobiology of pulmonary arterial hypertension (PAH). IL-6 plasma levels are elevated in PAH patients and closely linked to survival (1). Both increased IL-6 activity and gene knockout influence the development of, and resistance to, pulmonary hypertension in animal models (2–4). IL-6 can repress expression of BMPR2, a gene key to PAH risk (5). Footnotes This manuscript has recently been accepted for publication in the European Respiratory Journal . It is published here in its accepted form prior to copyediting and typesetting by our production team. After these production processes are complete and the authors have approved the resulting proofs, the article will move to the latest issue of the ERJ online. Please open or download the PDF to view this article. Conflicts of interests: The authors declare no conflicts of interest.