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Life
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Atherosclerosis: Pathogenesis, Clinical Advances and Future Perspectives
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Atherosclerosis: Pathogenesis, Clinical Advances and Future Perspectives

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Medical Research".

Deadline for manuscript submissions: 28 February 2026 | Viewed by 2675

Special Issue Editors

Dr. Damiano D’Ardes

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Guest Editor
"Clinica Medica" Institute, Department of Medicine and Aging Sciences, "G. D'Annunzio" University of Chieti-Pescara, 66100 Chieti, Italy
Interests: cardiovascular risk; lipid metabolism; metabolic diseases; ultrasound
Special Issues, Collections and Topics in MDPI journals
Dr. Ilaria Rossi

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Guest Editor
Clinica Medica Institute, European Center of Excellence on Atherosclerosis, Hypertension and Dyslipidemia, “G. D’Annunzio” University of Chieti-Pescara, 66100 Chieti, Italy
Interests: atherosclerosis; cardiovascular risk; cardiovascular prevention; hypertension; emergency medicine; lipidology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Biomedical science has shown that atherosclerosis is the protagonist of cardiovascular events. Even if many researchers have focused their attention on the physiopathological mechanisms that drive atherosclerosis, many aspects are still unknown. At the same time, physicians now have different therapeutic options compared to the past. This Special Issue aims to deepen the unresolved aspects regarding atherosclerosis and draw attention to the current therapeutic strategies and physiopathological mechanisms, inspiring researchers and physicians around the world to conduct new studies and provide the best possible treatment for their patients.

Dr. Damiano D’Ardes
Dr. Ilaria Rossi
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Life is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • atherosclerosis
  • cardiovascular risk
  • hypercholesterolemia
  • hypertension
  • inflammation
  • cardiovascular prevention

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Research

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20 pages, 3119 KiB  
Article
The Association of Histological Signs of Plaque Instability with Low eGFR, Higher Neutrophil-to-Lymphocyte Ratio, and Lower Serum MCP-1 Levels in Carotid Endarterectomy Patients—A Single-Center, Prospective Cohort Study
by Ioan Alexandru Balmos, Adina Huțanu, Adrian Vasile Muresan, Előd Ernő Nagy, Klara Brinzaniuc, Gyopár Beáta Molnár, Rita Szodorai and Emőke Horváth
Life 2025, 15(7), 1008; https://doi.org/10.3390/life15071008 - 25 Jun 2025
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Abstract
Background: Histological signs of carotid atheromatous plaque vulnerability, such as hemorrhage, neovascularization, atherothrombosis, and ulceration, develop against an unstable biological background. Declining renal function contributes to atherosclerotic progression and worsens cardiovascular outcomes. Methods: In a single-center prospective cohort study, we studied [...] Read more.
Background: Histological signs of carotid atheromatous plaque vulnerability, such as hemorrhage, neovascularization, atherothrombosis, and ulceration, develop against an unstable biological background. Declining renal function contributes to atherosclerotic progression and worsens cardiovascular outcomes. Methods: In a single-center prospective cohort study, we studied 41 endarterectomized patients with severe carotid atherosclerosis. The histological samples were stained with H&E to assess morphology and immunohistochemically labeled with antibodies for CRP and MMP-9 proteins. Complete blood count, the presence of serum biomarkers hsCRP, oxLDL, MCP-1, and MMP-9, and the level of eGFR were determined. Results: Twenty-eight patients with complicated plaques had significantly lower eGFR values: 79.5 (24–110) vs. 94 (69–114) (p = 0.004). Patients with eGFR > 90 mL/min/1.73m2 had a higher incidence of intraplaque hemorrhage and histologic complications of any cause (p = 0.012 and p = 0.003). Patients with bleeding and ulceration from the carotid plaque had a higher neutrophil/lymphocyte ratio. Significantly lower levels of MCP-1 were found in the serum of patients with massive inflammatory infiltrate of the carotid plaques, while serum levels of biomarkers like hsCRP, MMP-9, and oxLDL did not show differences in cases with plaque vulnerability. Conclusions: Signs of plaque vulnerability are associated with reduced renal function, a higher neutrophil/lymphocyte ratio, and lower serum levels of MCP-1 in advanced carotid artery stenosis disease. Full article
(This article belongs to the Special Issue Atherosclerosis: Pathogenesis, Clinical Advances and Future Perspectives)
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29 pages, 1689 KiB  
Systematic Review
Variability in Arterial Stiffness and Vascular Endothelial Function After COVID-19 During 1.5 Years of Follow-Up—Systematic Review and Meta-Analysis
by Danuta Loboda, Krzysztof S. Golba, Piotr Gurowiec, Aelita Bredelytė, Artūras Razbadauskas and Beata Sarecka-Hujar
Life 2025, 15(4), 520; https://doi.org/10.3390/life15040520 - 21 Mar 2025
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Abstract
Increasing long-term observations suggest that coronavirus disease 2019 (COVID-19) vasculopathy may persist even 1.5 years after the acute phase, potentially accelerating the development of atherosclerotic cardiovascular diseases. This study systematically reviewed the variability of brachial flow-mediated dilation (FMD) and carotid-femoral pulse wave velocity [...] Read more.
Increasing long-term observations suggest that coronavirus disease 2019 (COVID-19) vasculopathy may persist even 1.5 years after the acute phase, potentially accelerating the development of atherosclerotic cardiovascular diseases. This study systematically reviewed the variability of brachial flow-mediated dilation (FMD) and carotid-femoral pulse wave velocity (cfPWV) from the acute phase of COVID-19 through 16 months of follow-up (F/U). Databases including PubMed, Web of Science, MEDLINE, and Embase were screened for a meta-analysis without language or date restrictions (PROSPERO reference CRD42025642888, last search conducted on 1 February 2025). The quality of the included studies was assessed using the Newcastle–Ottawa Quality Scale. We considered all studies (interventional pre-post studies, prospective observational studies, prospective randomized, and non-randomized trials) that assessed FMD or cfPWV in adults (aged ≥ 18 years) with or after laboratory-confirmed COVID-19 compared with non-COVID-19 controls or that assessed changes in these parameters during the F/U. Twenty-one studies reported differences in FMD, and 18 studies examined cfPWV between COVID-19 patients and control groups during various stages: acute/subacute COVID-19 (≤30 days from disease onset), early (>30–90 days), mid-term (>90–180 days), late (>180–270 days), and very late (>270 days) post-COVID-19 recovery. Six studies assessed variability in FMD, while nine did so for cfPWV during the F/U. Data from 14 FMD studies (627 cases and 694 controls) and 15 cfPWV studies (578 cases and 703 controls) were included in our meta-analysis. FMD showed a significant decrease compared to controls during the acute/subacute phase (standardized mean difference [SMD]= −2.02, p < 0.001), with partial improvements noted from the acute/subacute phase to early recovery (SMD = 0.95, p < 0.001) and from early to mid-term recovery (SMD = 0.92, p = 0.006). Normalization compared to controls was observed in late recovery (SMD = 0.12, p = 0.69). In contrast, cfPWV values, which were higher than controls in the acute/subacute phase (SMD = 1.27, p < 0.001), remained elevated throughout the F/U, with no significant changes except for a decrease from mid-term to very late recovery (SMD= −0.39, p < 0.001). In the very late recovery, cfPWV values remained higher than those of controls (SMD = 0.45, p = 0.010). In the manuscript, we discuss how various factors, including the severity of acute COVID-19, the persistence of long-term COVID-19 syndrome, and the patient’s initial vascular age, depending on metrics age and cardiovascular risk factors, influenced the time and degree of FMD and cfPWV improvement. Full article
(This article belongs to the Special Issue Atherosclerosis: Pathogenesis, Clinical Advances and Future Perspectives)
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