Ion channels/pumps are essential regulators of innate immune cell function. Macrophages have been increasingly recognized to have phenotypic plasticity and location-specific functions in the lung. Transient receptor potential vanilloid 4 (TRPV4) function in lung injury has been shown to be stimulus- and cell-type specific. In the current review, we discuss the importance of TRPV4 in macrophages and its role in phagocytosis and cytokine secretion in acute lung injury/acute respiratory distress syndrome (ARDS). Furthermore, TRPV4 controls a MAPK molecular switch from predominately c-Jun N-terminal kinase, JNK activation, to that of p38 activation, that mediates phagocytosis and cytokine secretion in a matrix stiffness-dependent manner. Expanding knowledge regarding the downstream mechanisms by which TRPV4 acts to tailor macrophage function in pulmonary inflammatory diseases will allow for formulation of novel therapeutics.

离子通道/泵是先天免疫细胞功能的重要调节器。人们越来越认识到巨噬细胞在肺中具有表型可塑性和位置特异性功能。瞬时受体电位香草酸 4 (TRPV4) 在肺损伤中的功能已被证明具有刺激和细胞类型特异性。在本篇综述中，我们讨论了 TRPV4 在巨噬细胞中的重要性及其在急性肺损伤/急性呼吸窘迫综合征 (ARDS) 吞噬作用和细胞因子分泌中的作用。此外，TRPV4 控制 MAPK 分子从主要是 c-Jun N 端激酶、JNK 激活到 p38 激活的转换，以基质硬度依赖性方式介导吞噬作用和细胞因子分泌。扩展有关 TRPV4 在肺部炎症疾病中调节巨噬细胞功能的下游机制的知识，将有助于制定新的治疗方法。