Fatty acid nitroalkenes are reversibly-reactive electrophiles that are endogenously detectable at nM concentrations and display anti-inflammatory, pro-survival actions. These actions are elicited through the alteration of signal transduction proteins via a Michael addition on nucleophilic cysteine thiols. Nitrated fatty acids (NO₂-FAs), like 9- or 10-nitro-octadec-9-enolic acid, will act on signal transduction proteins directly or on key regulatory proteins to cause an up-regulation or down-regulation of the protein’s expression, yielding an anti-inflammatory response. These responses have been characterized in many organ systems, such as the cardiovascular system, with the pulmonary system less well defined. Macrophages are one of the most abundant immune cells in the lung and are essential in maintaining lung homeostasis. Despite this, macrophages can play a role in both acute and chronic lung injury due to up-regulation of anti-inflammatory signal transduction pathways and down-regulation of pro-inflammatory pathways. Through their propensity to alter signal transduction pathways, NO₂-FAs may be able to reduce macrophage activation during pulmonary injury. This review will focus on the implications of NO₂-FAs on macrophage activation in the lung and the signal transduction pathways that may be altered, leading to reduced pulmonary injury.

脂肪酸硝基烯烃是可逆反应的亲电子试剂，在 nM 浓度下可内源检测到，并具有抗炎、促生存作用。这些作用是通过亲核半胱氨酸硫醇上的迈克尔加成改变信号转导蛋白而引发的。硝化脂肪酸 (NO ₂ -FA)，如 9- 或 10-硝基-十八-9-烯醇酸，将直接作用于信号转导蛋白或关键调节蛋白，导致蛋白的上调或下调表达，产生抗炎反应。这些反应已在许多器官系统中得到表征，例如心血管系统，而肺系统则不太明确。巨噬细胞是肺部最丰富的免疫细胞之一，对于维持肺部稳态至关重要。尽管如此，由于抗炎信号转导途径的上调和促炎途径的下调，巨噬细胞可以在急性和慢性肺损伤中发挥作用。通过改变信号转导途径的倾向，NO ₂ -FA 可能能够减少肺损伤期间巨噬细胞的活化。本综述将重点关注 NO ₂ -FA 对肺部巨噬细胞活化的影响以及可能改变的信号转导途径，从而减少肺损伤。