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Updated: Sep 4, 2025

Ultrasound Assessment of Endothelial Function: A Technical Guideline of the Flow-mediated Dilation Test
Published on: April 27, 2016
Why is endothelial resilience key to maintain cardiac health?
Lukas S Tombor1,2, Stefanie Dimmeler3,4
1Institute of Cardiovascular Regeneration, Goethe University Frankfurt, Frankfurt, Germany.
Insights
Endothelial cells adapt to heart injury by changing their gene expression and appearance, aiding repair. This resilience is key to preventing long-term heart dysfunction after myocardial infarction.
Area of Science:
- Cardiovascular Biology
- Cellular and Molecular Medicine
- Regenerative Medicine
Background:
- Myocardial infarction (MI) causes ischemia and cardiomyocyte death, necessitating cardiac repair mechanisms.
- Endothelial cells are vital for restoring blood and nutrient supply to the injured heart.
- Understanding endothelial cell responses is crucial for developing therapies for heart disease.
Purpose of the Study:
- To summarize how endothelial cells adapt to cardiac injury and contribute to repair.
- To highlight factors influencing endothelial cell resilience and potential therapeutic targets.
- To elucidate the dynamic role of endothelial cells in cardiac regeneration post-injury.
Main Methods:
- Review of latest advances in single-cell multi-omics.
- Integration of genetic lineage tracing techniques.
- Analysis of transcriptional and phenotypical adaptations in endothelial cells.
Main Results:
- Endothelial cells exhibit significant transcriptional and phenotypical adaptation to the injured cardiac microenvironment.
- Observed changes include altered metabolic, mesenchymal, hematopoietic, and pro-inflammatory signatures.
- Many adaptive changes are transient, with endothelial cells reverting to a naive state post-injury resolution.
Conclusions:
- Endothelial cell resilience to acute stress is critical for preventing chronic cardiac dysfunction.
- Targeting intrinsic and microenvironmental factors can maintain a healthy cardiac microcirculation.
- The dynamic response of endothelial cells is a key contributor to cardiac repair and regeneration.
Abstract:
Myocardial injury as induced by myocardial infarction results in tissue ischemia, which critically incepts cardiomyocyte death. Endothelial cells play a crucial role in restoring oxygen and nutrient supply to the heart. Latest advances in single-cell multi-omics, together with genetic lineage tracing, reveal a transcriptional and phenotypical adaptation to the injured microenvironment, which includes alterations in metabolic, mesenchymal, hematopoietic and pro-inflammatory signatures. The extent of transition in mesenchymal or hematopoietic cell lineages is still debated, but it is clear that several of the adaptive phenotypical changes are transient and endothelial cells revert back to a naïve cell state after resolution of injury responses. This resilience of endothelial cells to acute stress responses is important for preventing chronic dysfunction. Here, we summarize how endothelial cells adjust to injury and how this dynamic response contributes to repair and regeneration. We will highlight intrinsic and microenvironmental factors that contribute to endothelial cell resilience and may be targetable to maintain a functionally active, healthy microcirculation.
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