Molecular Mechanisms Involved in the Pathophysiology of Sepsis: Role of Signaling Pathways

Sepsis is characterized as an aberrant and dysregulated physiological reaction to infection, resulting in severe and potentially fatal organ impairment. Globally, it poses a substantial public health burden, with nearly 48.9 million incidents and 11 million deaths annually. The core mechanisms of sepsis involve a cascade of systemic inflammation and dysregulation of the immune response, initiated by pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). Critical signaling pathways, such as TLR4, NF-κB, MAPK, JAK/STAT, and PI3K/Akt, drive the overproduction of inflammation-promoting molecules, oxidative damage, and organ harm. To obtain the necessary information, we searched the PubMed and Web of Science databases using the keywords sepsis, signal transduction pathway, and NF-κB-MAPK-PI3K/Akt-JAK/STAT-TLR-4. We primarily used articles published in the last 5 years. Focusing on these pathways offers potential treatment options to reduce the exaggerated inflammatory reaction and restore balanced immune function. Timely identification, tailored strategies, and the discovery of innovative biomarkers are essential for managing sepsis. This review explores the molecular pathways underlying the development and progression of sepsis.