“Dysregulation of lipid mediators in patients with frequent exacerbations of COPD” Marie Fisk, Esteban A. Gomez, Yuan Sun, Monika Mickute, Carmel McEniery, John R. Cockcroft, Charlotte Bolton, Jonathan Fuld, Joseph Cheriyan, Yasmin, William MacNee, Ruth Tal-Singer, Michael Polkey, Ian Wilkinson and Jesmond Dalli. ERJ Open Res 2025; 11: 00950-2023.

This article was originally published with an error in figure 4 in which the legend in the bottom left corner incorrectly defined the red triangle symbol as “Higher abundance in COPD stable” and the blue triangle symbol as “Lower abundance in COPD stable”. These have been corrected to “Higher abundance in exacerbators” and “Lower abundance in exacerbators”, respectively, in the figure below and in the article itself. We apologise for this error.

FIGURE 4.

Differential regulation of lipid mediator (LM) biosynthetic pathways in COPD patients with frequent exacerbations, compared with stable COPD patients. Analysis highlighting the relative regulation of mediators identified in figure 3 with VIP scores >1 and their biosynthetic pathways in stable COPD patients, compared with patients with exacerbations. Downregulation of ALOX5–ALOX15 pathways was observed in patients with frequent exacerbations, compared with stable COPD patients. There was general downregulation of the following LMs (lower abundance) in COPD patients with exacerbations (versus stable COPD patients): PGE₂, 15-epi-LXA₄, LXB₄, 5S, 15S-diHETE, 5S-12S-diHETE, RvE2, PDX, RvD1, RvD2, RvD3, RvD5 and 17R-RvD3, n3-RvD3. DHA: docosahexaenoic acid; n3-DPA: n3-docosapentaenoic acid; EPA: eicosapentaenoic acid; AA: arachidonic acid; LOX: lipoxygenase; COX: cyclooxygenase; CYP450: cytochromes P450; ALOX: arachidonate lipoxygenase; PG: prostaglandin; epi: epimer; LX: lipoxin; diHETE, dihydroxy-eicosatetraenoic acid; PDX: protecin DX (also referred to as 10S, 17S-dihydroxydocosahexaenoic acid (diHDHA)); Rv: resolvin.