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Updated: Feb 15, 2026
Isolation and Characterization of Microvesicles from Peripheral Blood
Published on: January 6, 2017
Microvesicles in Atherosclerosis and Angiogenesis: From Bench to Bedside and Reverse
Lina Badimon1,2, Rosa Suades1, Gemma Arderiu1
1Cardiovascular Research Center (ICCC) and CiberCV, Sant Pau Biomedical Research Institute (IIB-Sant Pau), Barcelona, Spain.
Insights
Microvesicles (MVs) are key players in atherosclerosis and cardiovascular disease (CVD) progression. Understanding their role in inflammation, thrombosis, and vascular remodeling offers potential for new diagnostic and therapeutic strategies in precision medicine.
Area of Science:
- Cardiovascular Biology
- Cellular Biology
- Biochemistry
Background:
- Atherosclerosis (AT) and cardiovascular disease (CVD) remain leading causes of mortality, driven by lipid accumulation, inflammation, and immune responses.
- Current treatments reduce cardiovascular event (CVE) risk, but significant unmet needs persist for identifying high-risk individuals and novel therapeutic targets.
- Microvesicles (MVs), shed from cells, are implicated in CVD development by mediating intercellular communication and cellular effects.
Purpose of the Study:
- To review the current understanding of microvesicle (MV) roles in atherosclerosis (AT) and cardiovascular disease (CVD).
- To highlight novel MV-mediated mechanisms in endothelial dysfunction, inflammation, oxidative stress, apoptosis, and coagulation.
- To discuss the potential prognostic, diagnostic, and therapeutic applications of cell-derived MVs in CVD.
Main Methods:
- Literature review focusing on microvesicles (MVs) in atherosclerosis (AT) and cardiovascular disease (CVD).
- Analysis of MV-mediated regulatory mechanisms including endothelial dysfunction, inflammation, oxidative stress, apoptosis, and coagulation.
- Examination of MV roles in vascular remodeling, angiogenesis, and neovascularization.
Main Results:
- MVs act as cellular effectors, facilitating biological information exchange and influencing all stages of AT and CVD progression.
- MV-mediated processes include endothelial dysfunction, vascular inflammation, oxidative stress, apoptosis, coagulation, and thrombosis.
- MVs impact vascular remodeling, endothelial-smooth muscle cell crosstalk, and AT-driven angiogenesis and neovascularization.
Conclusions:
- Microvesicles (MVs) are emerging regulators of biological functions in atherothrombosis, with significant implications for cardiovascular disease (CVD).
- MVs show promise as potential prognostic and diagnostic biomarkers, as well as therapeutic targets for CVD.
- Translating current findings on MV regulation and function into clinical practice requires substantial further research and effort.
Abstract:
Atherosclerosis (AT) is a progressive chronic disease involving lipid accumulation, fibrosis, and inflammation in medium and large-sized arteries, and it is the main cause of cardiovascular disease (CVD). AT is caused by dyslipidemia and mediated by both innate and adaptive immune responses. Despite lipid-lowering drugs have shown to decrease the risk of cardiovascular events (CVEs), there is a significant burden of AT-related morbidity and mortality. Identification of subjects at increased risk for CVE as well as discovery of novel therapeutic targets for improved treatment strategies are still unmet clinical needs in CVD. Microvesicles (MVs), small extracellular plasma membrane particles shed by activated and apoptotic cells have been widely linked to the development of CVD. MVs from vascular and resident cells by facilitating exchange of biological information between neighboring cells serve as cellular effectors in the bloodstream and play a key role in all stages of disease progression. This article reviews the current knowledge on the role of MVs in AT and CVD. Attention is focused on novel aspects of MV-mediated regulatory mechanisms from endothelial dysfunction, vascular wall inflammation, oxidative stress, and apoptosis to coagulation and thrombosis in the progression and development of atherothrombosis. MV contribution to vascular remodeling is also discussed, with a particular emphasis on the effect of MVs on the crosstalk between endothelial cells and smooth muscle cells, and their role regulating the active process of AT-driven angiogenesis and neovascularization. This review also highlights the latest findings and main challenges on the potential prognostic, diagnostic, and therapeutic value of cell-derived MVs in CVD. In summary, MVs have emerged as new regulators of biological functions in atherothrombosis and might be instrumental in cardiovascular precision medicine; however, significant efforts are still needed to translate into clinics the latest findings on MV regulation and function.
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