Sepsis is a complex and life-threatening syndrome arising from a dysregulated immune response to infection that can lead to severe organ dysfunction and increased mortality. This multifactorial condition is marked by intricate interactions between immune, inflammatory, and coagulation pathways, which together contribute to systemic effects and multiorgan damage. The aberrant immune activation seen in sepsis includes profound leukocyte activation, endothelial dysfunction, imbalanced coagulation leading to disseminated intravascular coagulation (DIC), and the production of both pro-inflammatory and anti-inflammatory mediators. These events culminate in pathological alterations that extend beyond the initial site of infection, adversely impacting distant tissues and organs. Early recognition and timely intervention are crucial to mitigate the progression of sepsis and its associated complications. This review aims to explore the underlying biological mechanisms, including host–pathogen interactions, immune dysregulation, and the cascade of systemic and organ-specific effects that define sepsis. By delving into the pathophysiological processes, we intend to provide insights into the determinants of multiorgan failure and inform strategies for therapeutic intervention. Understanding these mechanisms is pivotal for advancing clinical outcomes and reducing mortality rates associated with this critical condition.
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Hideaki Yamamoto
Tohoku University
Muhammad Usman
CMH Lahore Medical College and Institute of Dentistry
Aristides Koutrouvelis
The University of Texas Medical Branch at Galveston
Journal of Molecular Pathology
University of California, San Diego
The University of Texas Medical Branch at Galveston
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Yamamoto et al. (Thu,) studied this question.
synapsesocial.com/papers/68a3656a0a429f797332ba71 — DOI: https://doi.org/10.3390/jmp6030018
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