Prostaglandin and leukotriene metabolism in senescence (Homo sapiens)

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<?xml version="1.0" encoding="UTF-8"?> <Pathway xmlns="http://pathvisio.org/GPML/2013a" Name="Prostaglandin and leukotriene metabolism in senescence " Version="20210616" Organism="Homo sapiens"> <Comment Source="WikiPathways-description">Leukotrienes play an important role in the pathogenesis of inflammation. Just like prostaglandins, leukotrienes are synthesized from arachidonic acid that was cleaved from the membrane phospholipids (Wiley et al., 2019). ALOX12, ALOX15, ALOX5AP, LTC4S, LTA4H, ALOX15B and ALOX5, which are enzymes that conversion of arachidonic acid to either leukotriene A4 (LT4A) or Arachidonic acid 5-hydroperoxide (5-HPETE), are upregulated in senescence (Wiley et al., 2019; Häfner et al., 2019). The produced LTA4 can be converted into LTB4 or LTC4. LTC4 can then be consecutively cleaved into LTD4 and LTE4 (Suryadevara et al., 2020). All the mentioned leukotrienes are increased in cellular senescence and are thought to be part of the SASP (Lin &amp; Xu, 2020). LTD4 is of particular importance in cellular senescence due to its increased interaction with the cysteinyl leukotriene receptor 1 (CysLT1R) (Wei et al., 2018; Song et al., 2019). This interaction has various consequences, such as the release of intracellular Ca2+, an increase of p21 and it also inhibits sirtuin 1 (SIRT1). SIRT1 regulates the cell cycle by inhibiting the phosphorylation of p53 and the release of various cytokines (Wei et al., 2018). Therefore, it increases the release of pro-inflammatory cytokines and induce cellular senescence via the activation of p53 (Song et al., 2019). ALOX5 contributes to an increase in reactive oxygen species (ROS) (Catalano et al., 2005; Menna et al., 2010). These ROS are thought to activate p53 which binds to ALOX5 and further increases its action (Häfner et al., 2019). Moreover, ALOX5 uses Ca2+ as a cofactor and its increased intracellular concentration further promotes ALOX5’s action (Menna et al., 2010). LTB4 is also stimulates the production of ROS. ALOX5 then stimulates the phosphorylation of p53 and activates p21 (Menna et al., 2010; Catalano et al., 2005). This then causes the dephosphorylation of the retinoblastoma protein (RB1). 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