Endothelial to Mesenchymal Transition Represents a Key Link in the Interaction between Inflammation and Endothelial...

Area of Science:

• Vascular Biology and Endothelial Cell Function
• Cellular Phenotypic Plasticity
• Inflammation and Disease Pathogenesis

Background:

• Endothelial cells (ECs) exhibit heterogeneity and location-dependent properties, crucial for vascular homeostasis.
• Dynamic phenotypic switching in ECs, including endothelial to mesenchymal transition (EndMT), contributes to EC dysfunction and disease.
• Inflammation is a known inducer of EndMT, linking inflammatory responses to pathological vascular states.

Purpose of the Study:

• To review the current understanding of the interactions between inflammation, EndMT, and endothelial dysfunction.
• To focus on the regulatory mechanisms of essential signaling pathways involved in inflammation-induced EndMT.
• To highlight the role of EndMT in vascular dysfunction and disease development.

Main Methods:

• Literature review of current research on endothelial cell biology, inflammation, and EndMT.
• Analysis of studies investigating signaling pathways regulating EndMT.
• Synthesis of findings linking EndMT to vascular dysfunction and specific diseases.

Main Results:

• EndMT involves ECs losing endothelial markers and gaining mesenchymal phenotypes, driven by inflammatory processes.
• Inflammation-induced EndMT contributes to pathological conditions such as tissue fibrosis, pulmonary arterial hypertension, and atherosclerosis.
• Specific signaling pathways mediating inflammation-induced EndMT have been identified, though their precise role in vascular dysfunction requires further investigation.

Conclusions:

• EndMT is a critical mechanism linking inflammation to endothelial dysfunction and vascular diseases.
• Further research into the signaling pathways regulating EndMT is essential.
• Understanding these mechanisms may reveal novel therapeutic targets for vascular diseases.