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Updated: Jun 27, 2025
On-Chip Endothelial Inflammatory Phenotyping
Published on: July 21, 2012
Endothelial Reprogramming in Atherosclerosis
Lu Zhang1, Xin Wu1, Liang Hong1,2,3
1Department of Medicine, University of Illinois at Chicago, Chicago, IL 60612, USA.
Insights
Atherosclerosis involves endothelial reprogramming, where cells shift to a pro-inflammatory state. Targeting these changes and epigenetic factors may help prevent this vascular disease.
Area of Science:
- Cardiovascular Biology
- Vascular Cell Biology
- Molecular Medicine
Background:
- Atherosclerosis (AS) is a major cause of mortality, characterized by plaque formation in blood vessels.
- AS involves complex cellular interactions, with endothelial cells (ECs) playing a critical role.
- Endothelial dysfunction, termed 'endothelial reprogramming,' is key to AS initiation and progression.
Purpose of the Study:
- To review the role of endothelial cells in atherosclerosis pathogenesis.
- To summarize research on endothelial reprogramming in AS.
- To explore therapeutic strategies targeting endothelial changes.
Main Methods:
- Literature review of studies on endothelial cells in atherosclerosis.
- Analysis of mechanisms underlying endothelial reprogramming.
- Examination of epigenetic factors influencing endothelial function.
Main Results:
- Endothelial reprogramming involves a shift to a pro-inflammatory, proatherogenic state.
- Endothelial cell identity alterations include endothelial-to-mesenchymal transition (EndMT) and endothelial-to-immune cell-like transition (EndIT).
- Modulating epigenetic factors can impact endothelial reprogramming.
Conclusions:
- Endothelial reprogramming is a critical process in atherosclerosis development.
- Targeting endothelial reprogramming and epigenetic modifications offers potential therapeutic avenues for AS.
- Restoring endothelial balance is crucial for preventing AS progression.
Abstract:
Atherosclerosis (AS) is a severe vascular disease that results in millions of cases of mortality each year. The development of atherosclerosis is associated with vascular structural lesions, characterized by the accumulation of immune cells, mesenchymal cells, lipids, and an extracellular matrix at the intimal resulting in the formation of an atheromatous plaque. AS involves complex interactions among various cell types, including macrophages, endothelial cells (ECs), and smooth muscle cells (SMCs). Endothelial dysfunction plays an essential role in the initiation and progression of AS. Endothelial dysfunction can encompass a constellation of various non-adaptive dynamic alterations of biology and function, termed "endothelial reprogramming". This phenomenon involves transitioning from a quiescent, anti-inflammatory state to a pro-inflammatory and proatherogenic state and alterations in endothelial cell identity, such as endothelial to mesenchymal transition (EndMT) and endothelial-to-immune cell-like transition (EndIT). Targeting these processes to restore endothelial balance and prevent cell identity shifts, alongside modulating epigenetic factors, can attenuate atherosclerosis progression. In the present review, we discuss the role of endothelial cells in AS and summarize studies in endothelial reprogramming associated with the pathogenesis of AS.
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