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Endothelial Cell Function and Dysfunction in Critically Ill Children
Richard W Pierce1, John S Giuliano2, Jordan S Pober3
1Departments of Pediatrics and richard.pierce@yale.edu.
Insights
Endothelial cells (ECs) are crucial for vascular health and are implicated in critical illnesses. This review explores how ECs adapt, activate, or dysfunction during critical illness, impacting homeostasis and pathology.
Area of Science:
- Vascular Biology
- Critical Care Medicine
- Cellular Physiology
Background:
- Endothelial cells (ECs) form the inner lining of the vascular system.
- ECs regulate vital functions including blood flow, fluidity, and transport.
- Their widespread distribution implicates ECs in all critical illnesses.
Purpose of the Study:
- To review the adaptive and detrimental changes in endothelial cells during critical illness.
- To highlight the role of ECs in maintaining and disrupting homeostasis.
- To discuss clinical correlations and studies in critically ill children.
Main Methods:
- Review of existing literature on endothelial cell biology in critical illness.
- Analysis of EC activation and dysfunction pathways.
- Examination of clinical data and pediatric studies.
Main Results:
- ECs exhibit segmental differences and specific homeostatic roles.
- EC activation can restore homeostasis, while dysfunction contributes to pathology.
- Clinical correlations demonstrate the impact of EC changes in critical illness.
Conclusions:
- Endothelial cell adaptation and breakdown are central to critical illness.
- Understanding EC behavior is key to managing critical conditions.
- Research in critically ill children provides specific insights into EC roles.
Abstract:
Endothelial cells (ECs) line the lumen of the entire vascular system and actively regulate blood flow; maintain blood fluidity; control water, solute, and macromolecular transfer between blood and tissue; and modulate circulating immune cell recruitment and activation. These vital functions, combined with the broad anatomic distribution of ECs, implicate them in all forms of critical illness. The present article discusses how ECs adapt and break down during the course of critical illness. We first review the biology of ECs, highlighting the vascular segmental differences and their specific roles in the maintenance of homeostasis. We then discuss how ECs acquire new functions to restore local and systemic homeostasis (activation) as well as how breakdowns in EC functions (dysfunction) contribute to local and systemic pathologic responses, with clinical correlations. Lastly, how these processes have been studied in critically ill children is discussed.
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