Acute respiratory distress syndrome (ARDS) is an acute inflammatory pulmonary injury caused by multiple pathological factors.It mainly manifested as respiratory distress, intractable hypoxemia and respiratory failure, which significantly affect patient survival and health. The death of alveolar macrophage (AM) plays a pivotal role modulating the inflammatory response in ARDS. The loss of these cells affects other immune cell populations, advancing the inflammatory process and creating a positive feedback loop that intensifies cell death and lung injury. Therefore, this article reviews the molecular mechanisms of various cell death pathways, including apoptosis, necroptosis, autophagy, and ferroptosis, in acute lung injury, as well as their regulatory roles in the pathogenesis of ARDS inflammation. It also analyzes the underlying mechanisms based on recent research literature, thus providing new insights into the future treatment of ARDS.