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Interplay between Endoplasmic Reticulum Stress and Large Extracellular Vesicles (Microparticles) in Endothelial Cell
Aisha Osman1, Tarek Benameur2, Hesham M Korashy1
1Department of Pharmaceutical Sciences, College of Pharmacy, QU health, Qatar University, Doha 2713, Qatar.
Biomedicines
|October 15, 2020
Summary
Large extracellular vesicles (lEVs) contribute to endothelial dysfunction, a key factor in cardiovascular disease. Endoplasmic reticulum (ER) stress links lEVs to this dysfunction, highlighting a crucial molecular crosstalk.
Area of Science:
- Cellular Biology
- Pathophysiology
- Cardiovascular Science
Background:
- The unfolded protein response (UPR) is activated by protein misfolding in the endoplasmic reticulum (ER).
- Prolonged UPR leads to ER stress, contributing to chronic diseases like obesity, diabetes, and endothelial dysfunction.
- Endothelial dysfunction is a hallmark of cardiovascular disease, driven by apoptosis, insulin resistance, inflammation, and oxidative stress.
Purpose of the Study:
- To review the roles of large extracellular vesicles (lEVs) and ER stress in endothelial dysfunction.
- To discuss the molecular crosstalk and relationship between ER stress and lEVs in endothelial dysfunction.
Main Methods:
- Literature review summarizing current research on lEVs, ER stress, and endothelial dysfunction.
- Analysis of molecular mechanisms linking lEVs and ER stress to endothelial cell dysfunction.
Main Results:
- lEVs are emerging as significant contributors to endothelial cell dysfunction in metabolic diseases.
- ER stress is identified as a bridging molecular link between lEVs and endothelial dysfunction.
- lEVs carry molecular components from parent cells, acting as a fingerprint of cellular state.
Conclusions:
- lEVs play a critical role in mediating endothelial dysfunction, particularly in metabolic disease contexts.
- ER stress is a key molecular player connecting lEVs to endothelial dysfunction.
- Understanding the crosstalk between ER stress and lEVs is crucial for addressing cardiovascular disease pathogenesis.
Keywords:
cardiovascular diseasediabetesendoplasmic reticulum (ER) stressendothelial dysfunctionextracellular vesicles (EVs)metabolic syndromemicroparticles (MPs)More Related Videos
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