Dynamic Changes of Extracellular Matrix in Sepsis: A Review

During the pathogenesis of sepsis, extracellular matrix (ECM) impairment represents a critical pathological hallmark. The ECM not only plays pivotal roles in maintaining tissue architecture and physiological functions, but also actively participates in cellular signaling transduction and tissue repair mechanisms. Sepsisinduced systemic inflammatory responses and oxidative stress provoke ECM component degradation and structural remodeling, which, in turn, activate multiple intracellular and intercellular signaling cascades. Bioactive fragments derived from ECM degradation can function as signaling ligands that bind to specific cell surface receptors, triggering downstream pathways that regulate critical cellular processes, including survival, proliferation, migration, and inflammatory activation. The sustained activation of these signaling networks exerts profound pathophysiological consequences, potentially leading to vascular endothelial dysfunction, dysregulated immune cell hyperactivation, and coagulation system abnormalities. Furthermore, these signaling pathways mediate essential regulatory functions during the tissue remodeling phase in late-stage sepsis. While this dynamic ECM remodeling may facilitate tissue repair and regeneration, persistent dysregulation could result in maladaptive fibrosis and permanent organ dysfunction. Collectively, the ECM demonstrates multifaceted involvement in sepsis pathophysiology through its regulatory effects on cellular signaling, functional modulation, and tissue remodeling processes. This article systematically synthesizes current knowledge regarding ECM dynamics in sepsis pathogenesis.