Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) present significant challenges in critical care, with high mortality rates and limited treatment options. Alveolar epithelial type 2 (AT2) cells are central to lung repair and regeneration and play a vital role in maintaining lung homeostasis. However, the regulatory mechanisms governing AT2 cell fate during different stages of lung injury and repair remain incompletely understood. This review delves into the temporal and spatial heterogeneity of AT2 cells, highlighting their dynamic behavior in response to lung injury. We explore the pivotal role of AT2 cells across various stages of inflammation, repair, and fibrosis and discuss how these processes are influenced by factors such as aging, mechanical stress, and interactions within the alveolar microenvironment. This review also emphasizes the importance of integrating spatiotemporal multiomics approaches to uncover the molecular mechanisms underlying AT2 cell function and their potential therapeutic applications. Furthermore, we discuss novel strategies for enhancing the regenerative capacity of AT2 cells through targeted delivery systems, including protein, gene, and mitochondrial therapies. By advancing our understanding of AT2 cell biology and improving therapeutic approaches, we aim to pave the way for more effective treatments for lung injury diseases, particularly ALI and ARDS.

Sepsis, a life-threatening syndrome driven by dysregulated immune responses to infection, presents significant global health challenges with high mortality rates. Neutrophil extracellular traps (NETs), composed of deoxyribonucleic acid and antimicrobial proteins, play a dual role in sepsis pathogenesis. While NETs trap pathogens and enhance immune responses via antimicrobial activity and immune cell activation, their overproduction exacerbates tissue damage, coagulopathy, and organ dysfunction. This review explores the mechanisms of NET formation, including suicidal, vital, and noncanonical NETosis, and their regulation through pattern recognition receptors, complement systems, and chemokine signaling. The interplay between NETs and immune cells—such as macrophages, T cells, and platelets—is highlighted, emphasizing NETs’ role in both pathogen clearance and inflammatory injury. Excessive NETs contribute to sepsis-associated coagulopathy by activating platelets and damaging endothelial cells, while histones and proteases within NETs mediate cytotoxicity. Emerging therapeutic strategies targeting NETs, such as deoxyribonuclease, PAD4 inhibitors, and anti-inflammatory agents, show promise in preclinical studies but face clinical challenges due to their dual roles and off-target effects. Balancing NETs’ protective and pathological functions remains critical for sepsis management. This review aims to provide a comprehensive understanding of NETs in sepsis, offering insights for future research and clinical applications.

With the frequent occurrences of global large-scale and local violent terrorist events, local conflicts, explosions of inflammable and explosive materials and coal mine gas explosion, and other accidents, the incidence of explosion impact injury is increasing every year. The lung is one of the most vulnerable target organs in blast injury. Due to its high incidence, high mortality and lack of early effective evaluation methods, lung blast injury has attracted extensive attention in the medical field. The development of new protective materials for lung blast injury, early active injury assessment and real-time dynamic disease monitoring are of great significances for the prevention and treatment of patients. Here we discuss the clinical and research progress of lung blast injury based on basic (mechanism, protective materials, etc.) and clinical research hotspots (evaluation, ultrasonic diagnosis, etc.).