Core Insights - The research led by Sun Yat-sen University First Affiliated Hospital and Rutgers University has identified a transmembrane protein called NINJ1, which plays a significant role in the mechanical rupture of cell membranes, potentially offering new therapeutic avenues for treating sepsis and inflammation-related diseases [1][2] Group 1: Research Findings - The study reveals that NINJ1 significantly influences the probability of membrane rupture under mechanical stress across various cell types, indicating its role in maintaining membrane stability even in the absence of inflammatory pathways [1] - When NINJ1 is active, cell membranes are more prone to rupture under pressure; conversely, its knockout results in membranes that are unusually robust and pressure-resistant [2] Group 2: Clinical Implications - NINJ1 may serve as a novel target for regulating stress-related tissue damage, excessive inflammatory responses, and autoimmune diseases, particularly in conditions like lung injury, sepsis, or tumor microenvironments [2] - The potential therapeutic approach involves using small molecule drugs or nanoantibodies to inhibit NINJ1 activity, which could help control the release of damage-associated molecular patterns and reduce tissue destruction in sepsis-related inflammatory storms [2]