胞和其他心肌细胞之
-1β的产生触发了γδT细胞分泌IL-17A，这也参与了中性粒细胞浸润。304其他受体，例如血管紧张素 II 受体 1 型和腺苷 2 A 受体，介导巨噬细胞在血管损伤中的作用。305 , 306 巨噬细胞的细胞内信号传导 在没有 TGF-β 的情况下，吞噬作用会激活 Smad3。Smad3 的激活反过来会加速乳脂球 EGF 因子 8 (MFGE8) 的合成，从而启动抗炎级联反应，有助于巨噬细胞的抗炎表型，并最终保护心脏免遭心肌梗塞。Smad3 介导的促炎作用也与吞噬作用诱导的过氧
化物酶体增殖物激活受体 (PPAR) 表达的变化有关。307 巨噬细间的相互作用 M1 样电话号码列表巨噬细胞被证明会加重心肌梗塞后的心脏功能障碍。在心肌梗塞的情况下，M1 样巨噬细胞会分泌促炎性外泌体，将 miR-155 转移至内皮细胞。miR-155 被摄取并通过下调靶基因 Rac 家族小 GTPase 1 (RAC1)、p21 激活激酶 2 (PAK2)、Sirtuin 1 和 AMPKα2 导致血管生成抑制和心脏功能障碍。含有308 miR-155的外泌体也可以被心脏成纤维细胞摄取并抑制SOS1的表达，从而抑制成纤维细胞增殖和抑制细胞
https://lh5.googleusercontent.com/akNCmdCCmPlUUy322wuXydXBuglAvGSN05relsVYANKgW_NKYF2xhlen-OeEvnDGKFSX2xVSEQAXYre8bz0fekKhP-nRYEY_5r2wKmA0Q5L79XBnCYRnqkj9_eYBoe2V4oGAePUbQnFMP_jkge3TZZ0
因子信号传导1（SOCS1）的表达，从而增强炎症反应。309铁平衡对于维持正常的心血管状况至关重要。缺铁310和超负荷311都会导致心血管疾病。铁调素是铁的传感器和调节剂，由炎症性心脏巨噬细胞亚群合成和分泌，巨噬细胞中铁调素的特异性丢失会触发成年小鼠心肌梗死和新生小鼠心尖切除后的心肌细胞更新和心脏再生。Hepcidin 通过巨噬细胞中 STAT3 的磷酸化抑制修复性细胞因子 IL-4 和 IL-13 的分泌。第312章 IL-35
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