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Editorial
. 2020 Jan 15;201(2):138-140.
doi: 10.1164/rccm.201909-1790ED.

An Emotional Molecular Pathway in Pulmonary Hypertension-Alternative Complement System

Gabriele Grunig  1   2 , Nedim Durmus  2
Affiliations
Editorial

An Emotional Molecular Pathway in Pulmonary Hypertension-Alternative Complement System

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

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Figures

Figure 1.
Figure 1.
Schematic representation of the sequential experimental interrogation of the complement system presented in the article by Frid and colleagues (1). The complement components and interacting molecules are symbolized by colors and symbols. The shaded symbols denote factors that were found to be significantly different or have significant effects. The open symbols denote factors for which the study found no significance. The highly interactive complement network serves essential antimicrobial and immune surveillance functions by creating a membrane attack complex (red triangles) of C5b, C6, C7, C8, and C9 via a series of proteolytic reactions (5). The classical and lectin pathways (brown circles) lead to the generation of activated C4-C2 complex, which then activates C3, and in turn via activated C5 generates the membrane attack complex. The alternative pathway (blue squares) leads to activated C3 by using Cfb, Cfd, and Cfp, which then activates C5 and the membrane attack complex. C5 can also be activated in the alternative pathway via proteases of the coagulation system (kallikrein, plasmin [gray oval], and thrombin). By producing antibody (IgG; yellow triangles), B cells can activate the alternative pathway. Complement inhibitors (Cfh and CD55 [green boxes]) and serum protease inhibitors (serpins) are the endogenous blockers of the system. C = complement; CD = cluster of differentiation; KO = knockout; PAH = pulmonary arterial hypertension; PH = pulmonary hypertension.
See this image and copyright information in PMC

Comment on

References

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