Omics of endothelial cell dysfunction in sepsis

Area of Science:

• Molecular Biology
• Immunology
• Systems Biology

Background:

• Sepsis involves systemic inflammation, endothelial cell activation, and organ dysfunction.
• Endothelial cells exhibit organ-specific phenotypes crucial for targeted therapies.
• Omics technologies, particularly proteomics, offer mechanistic insights into cellular responses.

Purpose of the Study:

• To review the impact of sepsis pathophysiology on omics, focusing on endothelial cell proteomics.
• To explore the use of omics in defining septic endotypes and organ-specific endothelial cell dysfunction.
• To highlight the need for endothelial cell phenotype-specific proteomic analysis in sepsis.

Main Methods:

• Review of existing literature on sepsis, omics, and endothelial cell biology.
• Focus on proteomic analysis of mouse and human endothelial cells during sepsis/septic-like inflammation.
• Discussion of *in silico* modeling for analyzing omics data in sepsis.

Main Results:

• Sepsis induces complex proteomic changes in endothelial cells, varying by organ.
• Omics data can define septic endotypes and reveal organ-specific endothelial cell dysfunction.
• Proteomic analysis of endothelial cell phenotypes is essential for understanding sepsis heterogeneity.

Conclusions:

• Targeted therapies for sepsis require understanding organ-specific endothelial cell responses.
• Proteomic profiling of endothelial cell phenotypes is critical for defining sepsis subphenotypes.
• *In silico* modeling can integrate omics data to map sepsis response pathways.