Journal
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
Volume 24, Issue 21, Pages 12258-12271Publisher
WILEY
DOI: 10.1111/jcmm.15895
Keywords
barrier function; coagulopathy; glycocalyx; haemodynamics; inflammation; mechanotransduction; sepsis; shear stress
Categories
Funding
- National Institute of General Medical Sciences [R01GM121601, R01GM122775, R01GM116184, P30GM114731]
- National Institute of Allergy and Infectious Diseases [U19AI062629]
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Sepsis is a multifactorial syndrome primarily determined by the host response to an invading pathogen. It is common, with over 48 million cases worldwide in 2017, and often lethal. The sequence of events in sepsis begins with the damage of endothelium within the microvasculature, as a consequence of the inflammatory and coagulopathic responses to the pathogen that can progress to multiple organ failure and death. Most therapeutic interventions target the inflammation and coagulation pathways that act as an auto-amplified vicious cycle, which, if unchecked can be fatal. Normal blood flow and shear stress acting on a healthy endothelium and intact glycocalyx have anti-inflammatory, anticoagulant and self-repairing effects. During early stages of sepsis, the vascular endothelium and its glycocalyx become dysfunctional, yet they are essential components of resuscitation and recovery from sepsis. The effects of shear forces on sepsis-induced endothelial dysfunction, including inflammation, coagulation, complement activation and microcirculatory breakdown are reviewed. It is suggested that early therapeutic strategies should prioritize on the restoration of shear forces and endothelial function and on the preservation of the endothelial-glycocalyx barrier.
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