急性呼吸窘迫综合征（ARDS）是多病因引发的严重急性弥漫性炎症性肺损伤，以肺泡-毛细血管屏障破坏、肺水肿及低氧血症为特征，重症患者病死率高达35%～50%。当前治疗主要依赖机械通气与药物支持，但对肺泡-毛细血管屏障不可逆损伤尚缺乏特异性疗法，亟需探索新策略。细胞治疗凭借多重靶向作用已成为ARDS研究焦点。免疫调节：间充质干细胞（MSCs）和诱导多能干细胞（iPSCs）等通过分泌抗炎因子，如前列腺素E2（PGE2）、白细胞介素（IL）-10抑制核转录因子-κB（NF-κB）通路，降低肿瘤坏死因子-α（TNF-α）、IL-6等促炎因子水平，并调节免疫细胞平衡，减轻过度炎症反应；抗氧化应激：MSCs及外泌体通过激活Nrf2-ARE通路恢复线粒体功能，减少活性氧生成，缓解氧化损伤；组织修复：MSCs通过Wnt/β-catenin通路促进肺泡与血管内皮细胞增殖迁移，内皮祖细胞归巢修复血管内皮，降低通透性；抗纤维化与抗凋亡：MSCs分泌肝细胞生长因子抑制TGF-β/Smad通路，减少肌成纤维细胞活化，外泌体传递miRNAs抑制肺泡上皮细胞焦亡，延缓纤维化进程。针对新型冠状病毒肺炎相关ARDS的临床研究证实，MSCs、外泌体及调节性T细胞可有效调控炎症、改善氧合；脐带血及免疫-基质调节细胞等联合标准治疗亦展现协同潜力。但细胞治疗仍面临多重挑战：疗效异质性：受细胞来源、剂量、输注时机及患者基线病情影响，长期预后数据有限；安全风险：需警惕微栓塞、iPSCs致瘤性及免疫原性问题；技术瓶颈：细胞扩增、冻存及质控标准尚未统一，核心机制仍待阐明。本文系统综述了ARDS发病机制及细胞治疗的基础及临床研究进展，旨在为其治疗提供新思路。

Acute respiratory distress syndrome (ARDS) is a severe, acute and diffuse inflammatory lung injury arising from multiple etiologies, characterized by alveolar-capillary barrier disruption, pulmonary edema and hypoxemia, with mortality rates ranging from 35% to 50% among critically ill patients. Current management primarily relies on mechanical ventilation and supportive pharmacotherapy; however, there remains a lack of specific therapies for irreversible alveolar-capillary barrier damage, underscoring an urgent need for novel therapeutic strategies. Cellular therapy has emerged as a key focus in ARDS research owing to its multi-targeted actions: in terms of immunomodulation, mesenchymal stem cells (MSCs) and induced pluripotent stem cells (iPSCs) secrete anti-inflammatory factors such as prostaglandin E2 (PGE2) and interleukin (IL)-10, which inhibit the nuclear factor-κB (NF-κB) pathway, reduce levels of pro-inflammatory cytokines including tumor necrosis factor-α (TNF-α) and IL-6, and regulate immune cell homeostasis to mitigate excessive inflammatory responses; for antioxidative stress, MSCs and their exosomes restore mitochondrial function by activating the Nrf2-ARE pathway, diminish reactive oxygen species production and alleviate oxidative damage; regarding tissue repair, MSCs promote the proliferation and migration of alveolar epithelial cells and vascular endothelial cells via the Wnt/β-catenin pathway, while endothelial progenitor cells home to the injury site to repair the vascular endothelium and reduce vascular permeability; in relation to antifibrotic and anti-apoptotic effects, MSCs secrete hepatocyte growth factor to inhibit the TGF-β/Smad pathway and reduce myofibroblast activation, and exosomes deliver miRNAs to suppress alveolar epithelial pyroptosis and delay the fibrotic process. Clinical studies on corona virus disease 2019 (COVID-19)-associated ARDS have confirmed that MSCs, exosomes and regulatory T cells can effectively modulate inflammation and improve oxygenation, while umbilical cord blood, immunity-and-matrix regulatory cells and other cellular products, when combined with standard treatments, have demonstrated synergistic therapeutic potential. Nevertheless, cellular therapy for ARDS faces multiple challenges: therapeutic outcomes are influenced by cell source, dosage, timing of administration and patients’ baseline conditions, with limited long-term prognostic data available; safety concerns include microembolism, the tumorigenicity of iPSCs and immunogenicity issues; and standards for cell expansion, cryopreservation and quality control remain unstandardized, while the core mechanisms underlying therapeutic effects await further clarification. This article systematically reviews the pathogenesis of ARDS and advances in basic and clinical research on cellular therapy, aiming to provide new insights for future treatment strategies.