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Updated: Jan 3, 2026

A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation
Published on: December 9, 2021
Cross-Talk between Lipoproteins and Inflammation: The Role of Microvesicles
Gemma Chiva-Blanch1, Lina Badimon1,2
1Cardiovascular Program ICCC, Institut de Recerca Hospital Santa Creu i Sant Pau-IIB Sant Pau, Sant Antoni Maria Claret, 167, 08025 Barcelona, Spain.
Abstract:
Atherothrombosis is the principal underlying cause of cardiovascular disease (CVD). Microvesicles (MV) are small blebs originated by an outward budding at the cell plasma membranes, which are released in normal conditions. However, MV release is increased in pathophysiologic conditions such as CVD. Low density lipoprotein (LDL) and MV contribute to atherothrombosis onset and progression by promoting inflammation and leukocyte recruitment to injured endothelium, as well as by increasing thrombosis and plaque vulnerability. Moreover, (oxidized)LDL induces MV release and vice-versa, perpetuating endothelium injury leading to CVD progression. Therefore, MV and lipoproteins exhibit common features, which should be considered in the interpretation of their respective roles in the pathophysiology of CVD. Understanding the pathways implicated in this process will aid in developing novel therapeutic approaches against atherothrombosis.
Insights
Microvesicles (MV) and low-density lipoprotein (LDL) contribute to cardiovascular disease (CVD) by promoting inflammation and thrombosis. Understanding their interaction is key to developing new atherothrombosis therapies.
Area of Science:
- Cardiovascular Science
- Pathophysiology
- Molecular Biology
Background:
- Atherothrombosis, a major cause of cardiovascular disease (CVD), involves low-density lipoprotein (LDL) and microvesicles (MV).
- MV are cellular fragments released from cell membranes, with increased release observed in pathological conditions like CVD.
- Both LDL and MV contribute to atherothrombosis by promoting inflammation, leukocyte recruitment, and plaque instability.
Purpose of the Study:
- To elucidate the interconnected roles of microvesicles and lipoproteins in the pathophysiology of atherothrombosis.
- To highlight the reciprocal relationship between oxidized LDL and MV release in perpetuating endothelial injury.
- To identify therapeutic targets for novel treatments against atherothrombosis.
Main Methods:
- The study reviews existing literature on the molecular mechanisms linking MV and LDL in CVD.
- It analyzes the pathways involved in MV generation and their interaction with lipoproteins.
- The focus is on understanding the perpetuation of endothelial injury and atherothrombosis.
Main Results:
- MV and LDL share common features and actively contribute to atherothrombosis development and progression.
- Oxidized LDL induces MV release, and conversely, MV can promote LDL oxidation, creating a detrimental cycle.
- This interaction exacerbates endothelial dysfunction, inflammation, and thrombosis, driving CVD progression.
Conclusions:
- Microvesicles and lipoproteins play a critical, interconnected role in the pathogenesis of atherothrombosis.
- The reciprocal relationship between MV and LDL exacerbates endothelial injury and cardiovascular disease.
- Further understanding of these pathways is essential for developing effective therapeutic strategies against atherothrombosis.
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