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Vascular Pathologies in the Omics-Era

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 30 September 2025 | Viewed by 520

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Department of Neurological Surgery, Washington University School of Medicine, St. Louis, MO 63110, USA
Interests: cancer; stroke; epigenetics; molecular microbiology; genomics; nanobiotechnology; neurology
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Special Issue Information

Dear Colleagues,

Vascular pathology encompasses a spectrum of conditions impacting blood vessels and represents a pivotal area of inquiry within the burgeoning discipline of omics. This field involves a comprehensive analysis of diverse biomolecules on a large scale. In this omics era, researchers harness advanced technologies, including genomics, transcriptomics, proteomics, and metabolomics, in order to gain deeper insights into the intricate molecular mechanisms underlying vascular pathology. By scrutinizing the omics approaches of individuals with vascular ailments, researchers can pinpoint potential biomarkers for early detection, devise targeted therapeutic interventions, and enhance patient outcomes. The amalgamation of omics methodologies has yielded novel perspectives on the pathogenesis of vascular pathology and has forged a path toward tailored medical strategies to address these maladies. At its core, leveraging omics in exploring vascular pathology is anticipated to catalyze advancements in our comprehension and management of these intricate health challenges. This Special Issue invites original research and comprehensive reviews on the intersection of vascular diseases and omics.

Dr. Deepti Diwan
Guest Editor

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Keywords

  • vascular pathology
  • blood vessels
  • omics era
  • epigenetics
  • genomics
  • transcriptomics
  • proteomics
  • metabolomics

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Published Papers (1 paper)

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Research

17 pages, 1806 KiB  
Article
Non-Invasive Assessment of Vascular Damage Through Pulse Wave Velocity and Superb Microvascular Imaging in Pre-Dialysis Patients
by Julia Martín-Vírgala, Beatriz Martín-Carro, Sara Fernández-Villabrille, Belinda Fernández-Mariño, Elena Astudillo-Cortés, Minerva Rodríguez-García, Carmen Díaz-Corte, José Luis Fernández-Martín, Carlos Gómez-Alonso, Adriana S. Dusso, Cristina Alonso-Montes, Manuel Naves-Díaz, Sara Panizo and Natalia Carrillo-López
Biomedicines 2025, 13(3), 621; https://doi.org/10.3390/biomedicines13030621 - 4 Mar 2025
Viewed by 296
Abstract
Background/Objectives: Cardiovascular disease is the main cause of morbidity and mortality in Chronic Kidney Disease (CKD), so it is of great importance to find simple and non-invasive tools to detect vascular damage in pre-dialysis CKD patients. This study aimed to assess the [...] Read more.
Background/Objectives: Cardiovascular disease is the main cause of morbidity and mortality in Chronic Kidney Disease (CKD), so it is of great importance to find simple and non-invasive tools to detect vascular damage in pre-dialysis CKD patients. This study aimed to assess the applicability of non-invasive techniques to evaluate vascular damage in stages CKD-2 to CKD-5 and its progression after an 18-month follow-up using (A) carotid–femoral pulse wave velocity (PWV) to assess aortic stiffness and (B) Superb Microvascular Imaging (SMI) ultrasound to assess adventitial neovascularization compared with other traditional techniques to evaluate vascular damage, such as carotid intima–media thickness and Kauppila index. Methods: The study involved 43 CKD patients in stages CKD-2 to CKD-5 and a group of 38 sex- and age-matched controls, studied at baseline and at an 18-month follow-up. Age, sex, body mass index, arterial pressure, pharmacological treatments, and blood and urinary parameters were collected. Aortic stiffness was determined by carotid–femoral PWV and abdominal aortic calcification was assessed in lateral lumbar X-rays and quantified by the Kauppila index. Carotid intima–media thickness (cIMT), the number of carotid plaques, and adventitial neovascularization were evaluated by SMI. Results: Vascular impairment was mostly detected in CKD-4 and CKD-5 stages, with increased aortic stiffness measured by PWV and increased carotid plaques and adventitial neovascularization measured by SMI ultrasound. Furthermore, CKD-5 patients showed greater abdominal aortic calcification. Interestingly, CKD patients displayed a negative correlation between serum soluble Klotho (sKlotho) and cIMT. Finally, CKD patients showed no progression of vascular impairment after the 18-month follow-up, with the exception of carotid plaques. Conclusions: Performing non-invasive PWV and SMI ultrasound might be useful to evaluate vascular damage in CKD before entering dialysis, possibly helping to prevent cardiovascular events, although future studies should clarify the use of these techniques in clinical practice. Full article
(This article belongs to the Special Issue Vascular Pathologies in the Omics-Era)
Show Figures

Figure 1

Figure 1
<p>Assessment of vascular damage in the aorta in CKD patients grouped according to eGFR established in the KDIGO guidelines in CKD-2/3a, CKD-3b, CKD-4, and CKD-5 and in sex- and age-matched people from the general population (control group). (<b>a</b>) Aortic stiffness measured by pulse wave velocity (PWV) at baseline and (<b>b</b>) abdominal aortic quantification by Kauppila index based on a lateral radiograph of the lumbosacral spine after 18-month follow-up. Median and individual values for each group are shown. <sup>a</sup> <span class="html-italic">p</span> &lt; 0.05 and <sup>aaa</sup> <span class="html-italic">p</span> &lt; 0.005 versus the control.</p>
Full article ">Figure 2
<p>Superb Microvascular Imaging (SMI) ultrasound in carotid artery. (<b>a</b>) Number of carotid plaques, (<b>b</b>) carotid intima–media thickness (cIMT), (<b>c</b>) correlation between serum soluble Klotho (sKlotho) and cIMT, (<b>d</b>) number of carotid neovasa, and (<b>e</b>) carotid adventitial vasa vasorum (aVV) area in CKD patients grouped according to eGFR established in KDIGO guidelines in CKD-2/3a, CKD-3b, CKD-4, and CKD-5 and in sex- and age-matched people from general population (control group) at baseline. Median and individual values for each group are shown. <sup>a</sup> <span class="html-italic">p</span> &lt; 0.05, <sup>aaa</sup> <span class="html-italic">p</span> &lt; 0.005 versus control; <sup>b</sup> <span class="html-italic">p</span> &lt; 0.05, <sup>bbb</sup> <span class="html-italic">p</span> &lt; 0.005 versus CKD-2/3a and <sup>cc</sup> <span class="html-italic">p</span> &lt; 0.01 versus CKD-3b. Each shape represents CKD-2/3a (■), CKD-3b (●), CKD-4 (▲), and CKD-5 (♦).</p>
Full article ">Figure 3
<p>Correlation between carotid adventitial vasa vasorum (aVV) area and pulse wave velocity (PWV) in CKD patients grouped according to eGFR established in KDIGO guidelines in CKD-2/3a, CKD-3b, CKD-4, and CKD-5 and in sex- and age-matched people from general population (control group) at baseline. Each shape represents Control (○), CKD-2/3a (■), CKD-3b (●), CKD-4 (▲), and CKD-5 (♦).</p>
Full article ">
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