摘要
目的：本综述的主要重点是突出MK2激酶信号在p38MAPK途径中的当前和新兴的促炎作用，并提供对MK2抑制前景的详细评估，特别强调慢性炎症性气道疾病的病因，如哮喘，特发性肺纤维化，肺癌，急性肺损伤和急性呼吸窘迫综合征。 背景：MK2属于丝氨酸 - 苏氨酸激酶家族，通过Toll样受体信号通路在多种炎症条件下通过p38MAPK磷酸化直接激活应激和炎症信号。 MK2被认为是参与调节促炎（TNF-α，IL-6和IL-1β等）蛋白质的合成和释放的关键因子。已经显示靶向抑制MK2激酶显着减少这些细胞因子分子的产生和释放。因此，MK2已被确定为阻断这种促炎信号传导途径的有效策略（替代p38MAPK）。 结果：MK2的抑制可以导致与p38抑制剂相似或更好的功效，并且有趣地避免了p38抑制剂显示的全身毒性。因此，MK2一直是激烈的跨学科研究的焦点，其特异性抑制可以成为治疗慢性气道炎症性疾病的新颖和潜在的治疗策略。 结论：在理解和严格探索MK2激酶在炎症过程中的作用方面的有希望的进步可能有助于开发更新，更安全的治疗慢性气道炎症性疾病的治疗方法。
关键词: 丝裂原活化蛋白激酶活化蛋白激酶-2（MAPKAPK2或MK2），炎症，炎性气道疾病，p38MAPK途径，慢性肺炎，MK2抑制剂，哮喘。
图形摘要
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