“…Studies have found that Ghrelin has anti-inflammatory effects that inhibit Th1 and Th17 immune responses and promote Th2 and Tregs T cell immunity ( Dixit et al., 2004 ; Symonds et al., 2009 ; Stevanovic et al., 2012 ; Paoluzi et al., 2013 ; Xu et al., 2015 ). Current studies show that in the early and progressive stages of echinococcal infection, the JAK/STAT ( Liu et al., 2017 ; Yang et al., 2022 ), MEK/ERK1/2 ( Cheng et al., 2017 ; Lin et al., 2021 ) and PI3K/Akt/mTOR ( Covarrubias et al., 2015 ; Seoane et al., 2016 ; Yin et al., 2018 ; Wang et al., 2019 ; Yang et al., 2022 ) signaling pathways are upregulated and may be involved in regulating the parasitism and survival of Echinococcosis . High expression of Ghrelin could significantly upregulate the MEK/ERK1/2 ( Moreno et al., 2010 ; Kotta et al., 2022 ) and PI3K/Akt/mTOR ( Zhu et al., 2018 ; Petrescu et al., 2020 ; Zhang and Xie, 2020 ) signaling pathways, and inhibit NF-κB ( Zhou and Xue, 2009 ; Barazzoni et al., 2014 ; Mao et al., 2015b ; Mao et al., 2015a ) and TGF-β1/Smad3 ( Mao et al., 2015b ; Ezquerro et al., 2023 ) signaling pathways through interaction, significantly reducing the proinflammatory factors secreted by Th1-type cellular immunity, inhibiting the proliferation and activation of HSCs to restore the dynamic balance of MMP2 and TIMP1 and decrease the secretion of fibrotic cytokines α-SMA, collagen I and III, playing a role in reducing chronic inflammation and fibrosis formation in the liver.…”