Endothelial Dysfunction in Vascular Diseases

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 10 March 2026 | Viewed by 270

Special Issue Editor


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Guest Editor
Angiology and Noninvasive Vascular Diagnostics Unit, Department of Cardiovascular Sciences, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy
Interests: endothelial dysfunction; vascular diseases; atherosclerosis; hypertension

Special Issue Information

Dear Colleagues,

Endothelial dysfunction is a key factor in the development of cardiovascular and metabolic diseases, as it promotes vascular damage through oxidative stress, reduced nitric oxide bioavailability, and chronic inflammation. As the primary interface between blood and tissues, the endothelium plays a crucial role in vascular health by regulating vascular tone, permeability, coagulation, and immune responses. Under physiological conditions, this balance is maintained by mediators such as nitric oxide and prostacyclins; however, in the presence of chronic inflammation, hyperglycemia, dyslipidemia, and oxidative stress, this equilibrium is disrupted, leading to a pro-inflammatory and pro-thrombotic state.

This Special Issue will explore the complex interplay between endothelial dysfunction, inflammation, and metabolic dysregulation in vascular diseases, including, for example, atherosclerosis and hypertension. Emerging research on the role of inflammation in vascular injury and potential therapeutic strategies targeting endothelial repair and protection will also be highlighted. Early recognition of endothelial dysfunction through novel biomarkers and imaging techniques is increasingly regarded as essential for effective prevention and treatment. By advancing the understanding of these processes, this collection aims to promote innovative research and therapeutic approaches to reduce the global burden of cardiovascular diseases.

We invite the submission of original research articles and reviews elucidating the role of endothelial dysfunction in vascular pathology.

Dr. Antonio Nesci
Guest Editor

Manuscript Submission Information

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Keywords

  • endothelial dysfunction
  • vascular diseases
  • atherosclerosis
  • oxidative stress
  • nitric oxide
  • hypertension
  • vascular inflammation
  • endothelial repair

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Published Papers (1 paper)

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Review

20 pages, 931 KB  
Review
Cellular and Molecular Mechanisms of SARS-CoV-2 Spike Protein-Induced Endothelial Dysfunction
by Kelsey C. Muir, Dwight D. Harris, Meghamsh Kanuparthy, Jiayu Hu, Ju-Woo Nho, Christopher Stone, Debolina Banerjee, Frank W. Sellke and Jun Feng
Cells 2026, 15(3), 234; https://doi.org/10.3390/cells15030234 - 26 Jan 2026
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is initiated by the viral spike proteins, which are key structural components that mediate host cell binding and entry and alter downstream signaling through multiple interactions with endothelial surface receptors. Endothelial dysfunction is a central [...] Read more.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is initiated by the viral spike proteins, which are key structural components that mediate host cell binding and entry and alter downstream signaling through multiple interactions with endothelial surface receptors. Endothelial dysfunction is a central consequence of COVID-19, contributing to vascular inflammation, barrier disruption, thrombosis, and multi-organ injury affecting the pulmonary, cardiovascular, cerebral, and renal systems. Emerging evidence demonstrates that spike protein-mediated effects, independent of productive viral infection, disrupt endothelial homeostasis through angiotensin-converting enzyme 2 (ACE2) dysregulation, integrin engagement, altered calcium signaling, junctional protein remodeling, oxidative stress, and pro-inflammatory and pro-apoptotic pathways. This review is intentionally focused on spike (S) protein-driven mechanisms of endothelial dysfunction; pathogenic vascular effects attributed to other SARS-CoV-2 structural proteins, including the nucleocapsid (N) protein, are beyond the scope of this discussion. In this review, we synthesize current experimental and translational data detailing the molecular mechanisms by which the SARS-CoV-2 spike protein drives endothelial dysfunction across multiple organ systems and discuss potential therapeutic strategies aimed at preserving endothelial integrity in acute COVID-19 and its long-term vascular sequela. Full article
(This article belongs to the Special Issue Endothelial Dysfunction in Vascular Diseases)
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