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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: 31 August 2024 | Viewed by 294

Special Issue Editor


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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

Manuscript Submission Information

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Keywords

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

Published Papers (1 paper)

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15 pages, 1104 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
Viewed by 194
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
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