The clinical significance of endothelial dysfunction
Abstract
PURPOSE OF REVIEW: Endothelial dysfunction is thought to play a pivotal role in the development, progression, and clinical complications of atherosclerosis. Several recent studies have addressed the clinical implications of endothelial dysfunction for cardiovascular events, atherosclerosis, restenosis, and heart failure. Novel findings with respect to endothelial progenitor cells and their alteration by cardiovascular risk factors are characterized and potential therapeutic interventions to improve endothelial and endothelial progenitor cell function are discussed. RECENT FINDINGS: Over the past 5 years evidence has accumulated from clinical studies for a close association of the degree of endothelial dysfunction and clinical cardiovascular events in patients with cardiovascular risk factors, coronary disease, acute coronary syndrome, or heart failure. Understanding of the mechanisms leading to endothelial dysfunction has improved, including the notion that dysfunctional endothelial nitric oxide synthase, in part due to deficiency of the endothelial nitric oxide synthase cofactor tetrahydrobiopterin, likely plays an important role. Major progress has been made in understanding the role of endothelial progenitor cells, which likely contribute to both ischemia-induced neovascularization and endothelial regeneration after injury. Endothelial progenitor cell function is altered in patients with cardiovascular risk factors. SUMMARY: Recent research on endothelial and endothelial progenitor cell dysfunction supports their clinical significance and has led to important insights in the pathophysiology of cardiovascular disease and at the same time provides an important opportunity to develop novel therapeutic approaches. Endothelial function represents a valuable surrogate endpoint to assess the impact of therapeutic interventions.
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Impairment of endothelial function is a mechanism in the development of CVD and an independent predictor of CVD risk.
“Impairment of endothelial function is a mechanism in the development of CVD [73] and also an independent predictor of CVD risk [74].”
From Association between sleep deficiency and cardiometabolic disease: implications for health disparities (2016) · cites this paper as [73]
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- Authors
- Landmesser, U., & Drexler, H.
- Affiliations
- Medizinische Hochschule Hannover (DE)
- Corresponding author
- Landmesser, Ulf
- Drexler, Helmut
- ORCID
- Landmesser, Ulf
- Venue
- Current Opinion in Cardiology
- Published
- 2005-11
- Volume
- 20
- Issue
- 6
- Pages
- 547-551
- ISSN
- 0268-4705 (ISSN-L)
- OpenAlex
- W2089853948
- Cited by
- 142
- References
- 57
- Citations by year
- 2025: 1 · 2024: 3 · 2023: 4 · 2022: 5 · 2021: 2 · 2020: 7 · 2019: 5 · 2018: 5 · 2017: 6 · 2016: 9 · 2015: 4 · 2014: 8 · 2013: 11 · 2012: 12
- FWCI
- 1.00
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Opinion in Cardiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Keywords
- endothelial dysfunction, endothelial progenitor cells, atherosclerosis, cardiovascular risk factors, endothelial nitric oxide synthase, tetrahydrobiopterin, acute coronary syndrome, coronary disease, restenosis, heart failure, neovascularization, re-endothelialization, surrogate endpoints, endothelial function
- MeSH terms
- Angiotensin-Converting Enzyme Inhibitors, Cardiovascular Diseases, Endothelium, Vascular, Heart Failure, Humans, Life Style, Risk Factors, Stem Cells, Oxidative Stress, Nitric Oxide Synthase, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Angiotensin II Type 1 Receptor Blockers, Atherosclerosis
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