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Updated: May 20, 2026
Mouse Model of Alloimmune-induced Vascular Rejection and Transplant Arteriosclerosis
Published on: May 17, 2015
Signaling of endothelial cytoprotection in transplantation
1INSERM, UMR1064, Nantes, France. Beatrice.Charreau@univ-nantes.fr
Abstract:
A better knowledge of the processes by which endothelium can resist to cell death and adapt to injury by specific intracellular signaling pathways and dedicated protein regulation is a key step to understand how vascular inflammation/injury develops and how it is regulated. This review focuses on signaling pathways and molecular effectors that trigger the balance between endothelial cell activation and dysfunction. In addition to the canonical nuclear factor-κB (NF-κB), phosphatidyl inositol 3-kinase (PI-3K) and mitogen-activated protein kinases (MAPK) that orchestrated the inflammatory response and its termination we report here additive pathways such as Notch pathway and protein C/protease activated receptor (PAR) pathway that have been also reported to play a role in the control of EC activation and apoptosis. This review also provides an update of the characteristics of some established and novel protective molecules for the endothelium, identified in transplantation.
Insights
Understanding endothelial cell death and adaptation is crucial for vascular inflammation. This review details signaling pathways like Notch and Protein C, and protective molecules, aiding in managing endothelial cell activation and apoptosis.
Area of Science:
- Endothelial cell biology
- Vascular inflammation and injury
- Molecular signaling pathways
Background:
- Endothelial cells are vital for vascular health, and their response to injury influences inflammation.
- Understanding the mechanisms of endothelial cell survival and adaptation is key to regulating vascular inflammation.
Purpose of the Study:
- To review signaling pathways and molecular effectors controlling endothelial cell (EC) activation, dysfunction, and apoptosis.
- To highlight established and novel protective molecules for the endothelium, particularly in transplantation.
Main Methods:
- Literature review focusing on intracellular signaling pathways and protein regulation in endothelial cells.
- Analysis of canonical pathways (NF-κB, PI-3K, MAPK) and additive pathways (Notch, Protein C/PAR).
Main Results:
- Canonical pathways (NF-κB, PI-3K, MAPK) orchestrate inflammatory responses and their resolution.
- Notch and Protein C/PAR pathways also play significant roles in controlling EC activation and apoptosis.
- Identified established and novel protective molecules for endothelial cells.
Conclusions:
- A comprehensive understanding of EC signaling pathways is essential for managing vascular inflammation and injury.
- The Notch and Protein C/PAR pathways offer additional targets for therapeutic intervention.
- Protective molecules identified in transplantation research may hold broader therapeutic potential.
