Endothelial Dysfunction in Hypertension: Current Concepts and Clinical Implications
Open accessAbstract
Endothelium plays a fundamental role in the cardiovascular system, forming an interface between blood and adjacent tissues by regulating the vascular tone through the synthesis of nitric oxide, prostaglandins and other relaxing factors. Endothelial dysfunction is characterized by vasoconstriction, cell proliferation and shifting toward a proinflammatory and prothrombic state. In hypertension endothelial dysfunction may be involved in the initiation and development of vascular inflammation, vascular remodeling, and atherosclerosis and is independently associated with increased cardiovascular risk. Different conditions such as impaired vascular shear stress, inflammation and oxidative stress, activation of the renin angiotensin system have been described as important pathophysiological mechanisms involved in the development of endothelial dysfunction. The release of extracellular vesicles by neighboring cells in the vascular wall has emerged as an important regulator of endothelial function and with potential antihypertensive properties and beneficial effects by counteracting the hypertension mediated organ damage. Furthermore, macrovesicles are emerging as an innovative therapeutic approach for vascular protection, allowing the delivery of bioactive molecules, such as miRNA and drugs interacting with the renin angiotensin system. In this review we summarize the available evidence about the pathophysiological implications of endothelial dysfunction in cardiovascular diseases, focusing on hypertension and its sequelae, and the potential innovative therapeutic strategies targeting the endothelium with the aim to improve vascular function and remodeling.
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Controlling inflammation by reducing pro-inflammatory cytokines and blocking inflammatory pathways helps preserve vascular health and prevent hypertension.
“Moreover, controlling inflammation by reducing pro-inflammatory cytokines and blocking inflammatory pathways helps preserve vascular health and prevent hypertension [52].”
From Navigating the potential of algal peptides: health effects, market applications, and scientific challenges (2026) · cites this paper as [52]
The Conclusions (page unavailable) say that modulating vascular inflammation with RAS blockers and other antihypertensive drugs improves vascular function and remodeling. The therapeutic-intervention sections also describe reductions in inflammatory effects or markers, but do not establish that reducing pro-inflammatory cytokines and blocking inflammatory pathways prevents hypertension; their treatment discussion concerns vascular protection in hypertensive conditions. (LLM, conf=0.86)
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“…to prevent clot formation (Neubauer and Zieger 2022), regulating barrier permeability to control fluid and solute exchange (Sumpio et al. 2002), and modulating vascular tone through the production of vasoactive mediators such as nitric oxide and endothelin-1 (Gallo et al. 2021; Kostov 2021).”
- Authors
- Gallo, G., Volpe, M., & Savoia, C.
- Affiliations
- Azienda Ospedaliera Sant'Andrea (IT)
- Corresponding author
- Savoia, Carmine
- Venue
- Frontiers in Medicine
- Publisher
- Frontiers Media SA
- Published
- 2022-01-20
- Volume
- 8
- Pages
- 798958-798958
- ISSN
- 2296-858X (ISSN-L)
- PMC
- PMC8811286
- OpenAlex
- W4205645563
- Cited by
- 446
- References
- 82
- Citations by year
- 2026: 118 · 2025: 116 · 2024: 113 · 2023: 73 · 2022: 25
- FWCI
- 11.24
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
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- Frontiers in Medicine (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
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- IRIS Research product catalog (Sapienza University of Rome) (submittedVersion, cc-by)
- 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 › Extracellular vesicles in disease
- Keywords
- endothelial dysfunction, hypertension, nitric oxide, vascular inflammation, vascular remodeling, atherosclerosis, oxidative stress, shear stress, renin-angiotensin system, extracellular vesicles, microRNA delivery, cardiovascular risk
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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