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Editorial
. 2015 Oct 15;192(8):913-5.
doi: 10.1164/rccm.201507-1426ED.

Spotlight on Inflammation in Pulmonary Hypertension

Gabriele Grunig  1   2 , Nedim Durmus  1   2
Affiliations
Editorial

Spotlight on Inflammation in Pulmonary Hypertension

Gabriele Grunig et al. Am J Respir Crit Care Med. .
No abstract available

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Figures

Figure 1.
Figure 1.
Networks of mediators of inflammation in pulmonary arterial hypertension identified by Le Hiress and colleagues (2) and by Kumar and colleagues (1). The figure schematically shows several cell types in a pulmonary artery from pulmonary arterial hypertension lungs: endothelial cells (dark); leukocytes, among them T cells and macrophages (dark); and the remodeled artery wall of smooth muscle cells and connective tissue (gray shaded circle). The articles by Le Hiress and colleagues (2) and by Kumar and colleagues (1) focused on the contributions of the endothelial cell–CD74–MIF axis (2) and the bone marrow–derived leukocytes–IL-4–IL-13–transforming growth factor β axis (1), respectively. The groups identified shared cells (T cells), mediators (IL-6), and processes (leukocyte migration). Block arrows with question marks indicate potential additional links between the networks studied by the two research groups. Although these additional molecular links could exist, it is possible that the processes studied by Le Hiress and colleagues (2) and Kumar and colleagues (1) are distinct because the initializing events were distinct (hypoxia, monocrotaline, idiopathic pulmonary arterial hypertension, and heritable pulmonary arterial hypertension vs. Schistosoma-associated pulmonary arterial hypertension). ICAM-1 = intercellular adhesion molecule 1; MCT = monocrotaline; MIF = macrophage inhibitory factor; STAT6 = signal transducer and activator of transcription 6; TGF-β = transforming growth factor β; VCAM-1 = vascular cell adhesion protein 1.
See this image and copyright information in PMC

Comment on

References

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