Eicosanoids in tissue repair

Abstract

Trauma or infection can result in tissue damage, which needs to be repaired in a well‐orchestrated manner to restore tissue function and homeostasis. Lipid mediators derived from arachidonic acid (termed eicosanoids) play central and versatile roles in the regulation of tissue repair. Here, I summarize the current state‐of the‐art regarding the functional activities of eicosanoids in tissue repair responses during homeostasis and disease. I also describe how eicosanoids are produced during tissue damage and repair in a time‐, cell‐ and tissue‐dependent fashion. In particular, recent insights into the roles of eicosanoids in epithelial barrier repair are reviewed. Furthermore, the distinct roles of different eicosanoids in settings of pathological tissue repair such as chronic wounds, scarring or fibrosis are discussed. Finally, an outlook is provided on how eicosanoids may be targeted by future therapeutic strategies to achieve physiological tissue repair and prevent scarring and loss of tissue function in various disease contexts.

Neutrophil–macrophage cooperation and its impact on tissue repair

“…This proremodeling phenotype resembles the phenotype macrophages take on following in vitro stimulation with IL‐4, and these cells are herein referred to as M(IL‐4) to follow the recent restructuration of the macrophage polarization appellation (Figure ). Proremodeling macrophages are an important source of anti‐inflammatory mediators including lipoxins and resolvins, chemokines, matrix‐metalloproteinases and growth factors (please see the review by Esser von‐Bieren on lipid mediators in repair in this issue). Among the latter, platelet‐derived growth factor and transforming growth factor beta stimulate the proliferation and differentiation of stromal cells as well as promote the synthesis of ECM components while insulin‐like growth factor and vascular endothelial growth factor alpha are required for initiating the proliferative phase of repair …”

Driving regeneration, instead of healing, in adult mammals: the decisive role of resident macrophages through efferocytosis

“…Among the other signaling molecules released during inflammation are the prostaglandins. PGE2 and D2 are indeed produced in a time-dependent fashion, and actively contribute to tissue repair 32 , 33 . In agreement with our data, the inhibition of the PGE2-degrading enzyme, thus leading to an increase in PGE2 levels, has been shown to promote tissue repair in a mouse model of liver injury 34 .…”

Annexin A1 Regulates NLRP3 Inflammasome Activation and Modifies Lipid Release Profile in Isolated Peritoneal Macrophages

“…The major lipid classes can be categorized as fatty acyls, glycerolipids, glycerophospholipids, sphingolipids, sterol lipids, prenol lipids, saccharolipids, and polyketides [37]. In addition, cells can synthesize lipids, such as the eicosanoids, which are derived by the arachidonic acid oxidation and represented by prostaglandins, leukotrienes, thromboxanes, lipoxins, and epoxyeicosatrienoic acids [38]. By providing the exact mass, retention time, and elution profile, our study presents new data about the lipidomic profile of the supernatant of macrophages after NLRP3 activation by nigericin.…”