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Endothelial Dysfunction: Molecular Mechanisms and Therapeutic Strategies
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Endothelial Dysfunction: Molecular Mechanisms and Therapeutic Strategies

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 February 2025 | Viewed by 3152

Special Issue Editor

Prof. Dr. Nunzia D’Onofrio

E-Mail Website
Guest Editor
Department of Precision Medicine, University of Campania Luigi Vanvitelli, Via L. de Crecchio 7, 80138 Naples, Italy
Interests: endothelial dysfunction; atherosclerosis; epigenetic; oxidative stress; inflammation; mitochondria; natural compounds; senescence; cardiovascular
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

It is essential for tissue health and function to have a functional endothelium and vasculature. Dysfunctional endothelial cells lose their ability to maintain homeostasis, leading to deleterious consequences for both vessels and the organs they supply. Endothelial dysfunction may occur as a consequence, as well as contribute to the pathogenesis of many chronic degenerative diseases, including atherosclerosis, hypertension, and type II diabetes. Endothelial dysfunction is a complex process involving many signaling pathways depending on organ, vessel size, and sex, among other factors. The elucidation of the molecular mechanisms involved in endothelial dysfunction is crucial for the development of efficient therapies to improve endothelial function and vascular homeostasis in disease.

Contributions to this Special Issue should aim to provide insight into the mechanisms through which endothelial cell dysfunction contributes to the pathogenesis of vascular complications and diseases. A better understanding of these mechanisms would provide an opportunity to prevent and treat vascular disorders triggered and advanced by endothelial dysfunction.

Prof. Dr. Nunzia D’Onofrio
Guest Editor

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Keywords

  • endothelial dysfunction
  • inflammation
  • mitochondria
  • redox homeostasis
  • metabolic impairment
  • epigenetic
  • sirtuin
  • microRNA
  • senescence

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Published Papers (3 papers)

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15 pages, 8406 KiB  
Article
MiR-148a-3p/SIRT7 Axis Relieves Inflammatory-Induced Endothelial Dysfunction
by Camilla Anastasio, Isabella Donisi, Antonino Colloca, Nunzia D’Onofrio and Maria Luisa Balestrieri
Int. J. Mol. Sci. 2024, 25(10), 5087; https://doi.org/10.3390/ijms25105087 - 7 May 2024
Cited by 3 | Viewed by 1185
Abstract
In endothelial cells, miR-148a-3p is involved in several pathological pathways, including chronic inflammatory conditions. However, the molecular mechanism of miR-148a-3p in endothelial inflammatory states is, to date, not fully elucidated. To this end, we investigated the involvement of miR-148a-3p in mitochondrial dysfunction and [...] Read more.
In endothelial cells, miR-148a-3p is involved in several pathological pathways, including chronic inflammatory conditions. However, the molecular mechanism of miR-148a-3p in endothelial inflammatory states is, to date, not fully elucidated. To this end, we investigated the involvement of miR-148a-3p in mitochondrial dysfunction and cell death pathways in human aortic endothelial cells (teloHAECs) treated with interleukin-6 (IL-6), a major driver of vascular dysfunction. The results showed that during IL6-activated inflammatory pathways, including increased protein levels of sirtuin 7 (SIRT7) (p < 0.01), mitochondrial stress (p < 0.001), and apoptosis (p < 0.01), a decreased expression of miR-148a-3p was observed (p < 0.01). The employment of a miR-148a mimic counteracted the IL-6-induced cytokine release (p < 0.01) and apoptotic cell death (p < 0.01), and ameliorated mitochondria redox homeostasis and respiration (p < 0.01). The targeted relationship between miR-148a-3p and SIRT7 was predicted by a bioinformatics database analysis and validated via the dual-luciferase reporter assay. Mechanistically, miR-148a-3p targets the 3′ untranslated regions of SIRT7 mRNA, downregulating its expression (p < 0.01). Herein, these in vitro results support the role of the miR-148a-3p/SIRT7 axis in counteracting mitochondrial damage and apoptosis during endothelial inflammation, unveiling a novel target for future strategies to prevent endothelial dysfunction. Full article
(This article belongs to the Special Issue Endothelial Dysfunction: Molecular Mechanisms and Therapeutic Strategies)
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11 pages, 269 KiB  
Article
Anti TNF-Alpha Treatment Improves Microvascular Endothelial Dysfunction in Rheumatoid Arthritis Patients
by Alexandru Caraba, Oana Stancu, Viorica Crișan and Doina Georgescu
Int. J. Mol. Sci. 2024, 25(18), 9925; https://doi.org/10.3390/ijms25189925 - 14 Sep 2024
Viewed by 743
Abstract
Nailfold capillaroscopy is a non-invasive investigation, which allows for the study of the microvasculature (anatomical and functional). Rheumatoid arthritis (RA) is associated with a high risk of cardiovascular atherosclerotic diseases, with endothelial dysfunction (macrovascular and microvascular) representing the first step in atherosclerosis development. [...] Read more.
Nailfold capillaroscopy is a non-invasive investigation, which allows for the study of the microvasculature (anatomical and functional). Rheumatoid arthritis (RA) is associated with a high risk of cardiovascular atherosclerotic diseases, with endothelial dysfunction (macrovascular and microvascular) representing the first step in atherosclerosis development. The aim of this study is represented by the assessment of microvascular endothelial dysfunction in RA patients by means of nailfold capillaroscopy and to assess its evolution after a period of 12 months of anti TNF-alpha treatment. The study included 70 consecutive patients with RA and 70 healthy subjects, matched for age and gender, as the control group. Rheumatoid factor, anti-cyclic citrullinated peptide antibodies, serum TNF-α, C reactive protein, and erythrocytes sedimentation rate were evaluated in all patients, but in controls, only rheumatoid factor, serum TNF-α, C reactive protein, and erythrocytes sedimentation rate were measured. The RA activity was measured by DAS28. Nailfold capillaroscopy was carried out in all patients and controls, determining the baseline nailfold capillary density (Db), nailfold capillary density during reactive hyperemia (Dh), and nailfold capillary density after venous congestion (Dc). Data were presented as mean ± standard deviation. Statistical analysis was performed using ANOVA and Pearson’s correlation, with p < 0.05 being statistically significant. Db, Dh, and Dc were lower in RA patients than in controls (p < 0.0001), correlating with RA activity and TNF-α (p < 0.05). After 12 months of anti TNF-α treatment, microvascular endothelial dysfunction improved (p < 0.0001). Microvascular endothelial dysfunction can be assessed by nailfold capillaroscopy, with anti TNF-α medication contributing to its improvement. Full article
(This article belongs to the Special Issue Endothelial Dysfunction: Molecular Mechanisms and Therapeutic Strategies)
17 pages, 2996 KiB  
Article
Limosilactobacillus reuteri HY7503 and Its Cellular Proteins Alleviate Endothelial Dysfunction by Increasing Nitric Oxide Production and Regulating Cell Adhesion Molecule Levels
by Hyejin Jeon, Daehyeop Lee, Joo-Yun Kim, Jae-Jung Shim and Jae-Hwan Lee
Int. J. Mol. Sci. 2024, 25(20), 11326; https://doi.org/10.3390/ijms252011326 - 21 Oct 2024
Viewed by 718
Abstract
Endothelial dysfunction, which is marked by a reduction in nitric oxide (NO) production or an imbalance in relaxing and contracting factor levels, exacerbates atherosclerosis by promoting the production of cell adhesion molecules and cytokines. This study aimed to investigate the effects of Limosilactobacillus [...] Read more.
Endothelial dysfunction, which is marked by a reduction in nitric oxide (NO) production or an imbalance in relaxing and contracting factor levels, exacerbates atherosclerosis by promoting the production of cell adhesion molecules and cytokines. This study aimed to investigate the effects of Limosilactobacillus reuteri HY7503, a novel probiotic isolated from raw milk, on endothelial dysfunction. Five lactic acid bacterial strains were screened for their antioxidant, anti-inflammatory, and endothelium-protective properties; L. reuteri HY7503 had the most potent effect. In a mouse model of angiotensin II-induced endothelial dysfunction, L. reuteri HY7503 reduced vascular thickening (19.78%), increased serum NO levels (226.70%), upregulated endothelial NO synthase (eNOS) expression in the aortic tissue, and decreased levels of cell adhesion molecules (intercellular adhesion molecule-1 [ICAM-1] and vascular cell adhesion molecule-1 [VCAM-1]) and serum cytokines (tumor necrosis factor-alpha [TNF-α] and interleukin-6 [IL-6]). In TNF-α-treated human umbilical vein endothelial cells (HUVECs), L. reuteri HY7503 enhanced NO production and reduced cell adhesion molecule levels. In HUVECs, surface-layer proteins (SLPs) were more effective than extracellular vesicles (exosomes) in increasing NO production and decreasing cell adhesion molecule levels. These findings suggested that L. reuteri HY7503 may serve as a functional probiotic that alleviates endothelial dysfunction. Full article
(This article belongs to the Special Issue Endothelial Dysfunction: Molecular Mechanisms and Therapeutic Strategies)
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