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Molecular Mechanisms, Pathogenesis, and Novel Therapeutic Strategies in Cardiovascular Disease
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Molecular Mechanisms, Pathogenesis, and Novel Therapeutic Strategies in Cardiovascular Disease

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: closed (30 April 2024) | Viewed by 5006

Special Issue Editor

Dr. Dai Yamanouchi

E-Mail Website
Guest Editor
Division of Vascular Surgery, Department of Surgery, University of Wisconsin School of Medicine and Public Health, 1111 Highland Avenue, Madison, WI 53705, USA
Interests: aneurysm; vascular biology; angiogenesis; intimal hyperplasia; macrophage; osteoclastogenesis; MMPs
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Aneurysms, characterized by the localized dilation of blood vessels, pose a significant health risk due to the potential for rupture and life-threatening hemorrhage. In recent years, there has been growing interest in understanding the molecular mechanisms underlying the development and progression of aneurysms. This Special Issue aims to highlight recent advances in aneurysm research, focusing on the molecular aspects of aneurysm formation, progression, and novel therapeutic strategies.

In this Special Issue of the International Journal of Molecular Sciences, we invite authors to submit original research articles, reviews, and perspectives that delve into the molecular underpinnings of aneurysm formation and progression, specifically in relation to cardiovascular disease. Topics of interest include, but are not limited to, vascular remodeling, extracellular matrix degradation, the role of inflammatory signaling pathways, and the identification of novel molecular targets for therapy.

We particularly encourage submissions that provide in-depth insights into the molecular mechanisms of aneurysm pathobiology and the intricate interplay between various cellular and molecular factors contributing to aneurysm development. Contributions exploring innovative therapeutic approaches, such as gene therapy, stem cell therapy, and pharmacological interventions targeting specific molecular pathways, are also welcome.

By assembling a diverse collection of high-quality articles, this Special Issue aims to advance our understanding of the complex molecular landscape governing aneurysm formation and progression in cardiovascular disease and to inspire further research in this rapidly evolving field.

Dr. Dai Yamanouchi
Guest Editor

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • aneurysm pathobiology
  • vascular remodeling
  • extracellular matrix degradation
  • inflammatory signaling pathways
  • molecular targets for therapy
  • autophagy
  • macrophage
  • inflammation
  • immune cell regulation
  • age-related diseases
  • therapeutic implications

Published Papers (4 papers)

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Research

13 pages, 3271 KiB  
Article
Antioxidants and azd0156 Rescue Inflammatory Response in Autophagy-Impaired Macrophages
by Abdalla Elbialy, Mai Kitauchi and Dai Yamanouchi
Int. J. Mol. Sci. 2024, 25(1), 169; https://doi.org/10.3390/ijms25010169 - 21 Dec 2023
Viewed by 901
Abstract
Autophagy is a lysosomal degradation system that eliminates and recycles damaged intracellular organelles and proteins. Inflammatory macrophages play a critical role in the development of various age-related inflammatory illnesses such as abdominal aortic aneurysm, atherosclerosis, and rheumatoid arthritis; therefore, identifying the mechanisms that [...] Read more.
Autophagy is a lysosomal degradation system that eliminates and recycles damaged intracellular organelles and proteins. Inflammatory macrophages play a critical role in the development of various age-related inflammatory illnesses such as abdominal aortic aneurysm, atherosclerosis, and rheumatoid arthritis; therefore, identifying the mechanisms that cause macrophage inflammation is crucial for a better understanding of and developing therapeutics for inflammatory diseases. Previous research has linked autophagy to macrophage inflammation; Atg16L1-deficient macrophages increase IL-1 and IL-18 production via inflammasome activation. In this study, however, we show an alternative pathway of macrophage inflammation in an autophagy-deficient environment. We found that inhibiting autophagy in THP1 macrophages progressively increased the expression of p65-mediated inflammatory genes. This effect was reversed by treatment with antioxidants or azd0156, an ataxia telangiectasia mutated (ATM) inhibitor. In addition, our results showed that M1 macrophages inhibit autophagy and induce DNA damage, whereas M2 macrophages activate autophagy and reduce DNA damage. Importantly, the chemical activation of autophagy or ATM inhibition during M1 polarization reduced the M1 phenotype and inflammation, whereas inhibiting autophagy during M2 polarization also reduced the M2 phenotype. Thus, our findings highlight the importance of the autophagy–ATM pathway in driving macrophage inflammation. Full article
(This article belongs to the Special Issue Molecular Mechanisms, Pathogenesis, and Novel Therapeutic Strategies in Cardiovascular Disease)
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11 pages, 2811 KiB  
Article
Vascular Ultrasound for In Vivo Assessment of Arterial Pathologies in a Murine Model of Atherosclerosis and Aortic Aneurysm
by Alexander Hof, Henning Guthoff, Maysam Ahdab, Max Landerer, Jasper Schäkel, Jana Niehues, Maximilian Schorscher, Oscar Zimmermann, Holger Winkels, Philipp von Stein, Simon Geißen, Stephan Baldus, Matti Adam, Martin Mollenhauer and Dennis Mehrkens
Int. J. Mol. Sci. 2023, 24(20), 15261; https://doi.org/10.3390/ijms242015261 - 17 Oct 2023
Viewed by 1032
Abstract
Vascular diseases like atherosclerosis and abdominal aortic aneurysm (AAA) are common pathologies in the western world, promoting various potentially fatal conditions. Here, we evaluate high-resolution (HR) ultrasound in mouse models of atherosclerosis and AAA as a useful tool for noninvasive monitoring of early [...] Read more.
Vascular diseases like atherosclerosis and abdominal aortic aneurysm (AAA) are common pathologies in the western world, promoting various potentially fatal conditions. Here, we evaluate high-resolution (HR) ultrasound in mouse models of atherosclerosis and AAA as a useful tool for noninvasive monitoring of early vascular changes in vivo. We used Apolipoprotein E-deficient (ApoE−/−) mice as an atherosclerosis model and induced AAA development by the implementation of Angiotensin II-releasing osmotic minipumps. HR ultrasound of the carotid artery or the abdominal aorta was performed to monitor vascular remodeling in vivo. Images were analyzed by speckle tracking algorithms and correlated to histological analyses and subsequent automated collagen quantification. Consistent changes were observed via ultrasound in both models: Global radial strain (GRS) was notably reduced in the AAA model (23.8 ± 2.8% vs. 12.5 ± 2.5%, p = 0.01) and in the atherosclerotic mice (20.6 ± 1.3% vs. 15.8 ± 0.9%, p = 0.02). In mice with AAA, vessel distensibility was significantly reduced, whereas intima–media thickness was increased in atherosclerotic mice. The area and collagen content of the tunica media were increased in diseased arteries of both models as measured by automated image analysis of Picrosirius Red-stained aortic sections. Correlation analysis revealed a strong correlation of multiple parameters, predicting early vascular damage in HR ultrasound and histological examinations. In conclusion, our findings underscore the potential of HR ultrasound in effectively tracing early alterations in arterial wall properties in murine models of atherosclerosis and AAA. Full article
(This article belongs to the Special Issue Molecular Mechanisms, Pathogenesis, and Novel Therapeutic Strategies in Cardiovascular Disease)
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20 pages, 5005 KiB  
Article
Allicin, an Emerging Treatment for Pulmonary Arterial Hypertension: An Experimental Study
by José L. Sánchez-Gloria, Constanza E. Martínez-Olivares, Leonardo Del Valle-Mondragón, Fernando Cortés-Camacho, Oscar R. Zambrano-Vásquez, Rogelio Hernández-Pando, Fausto Sánchez-Muñoz, Laura G. Sánchez-Lozada and Horacio Osorio-Alonso
Int. J. Mol. Sci. 2023, 24(16), 12959; https://doi.org/10.3390/ijms241612959 - 19 Aug 2023
Viewed by 1400
Abstract
We assessed whether allicin, through its antihypertensive and antioxidant effects, relieves vascular remodeling, endothelial function, and oxidative stress (OS), thereby improving experimental pulmonary arterial hypertension (PAH). Allicin (16 mg/kg) was administered to rats with PAH (monocrotaline 60 mg/kg). Allicin encouraged body weight gain [...] Read more.
We assessed whether allicin, through its antihypertensive and antioxidant effects, relieves vascular remodeling, endothelial function, and oxidative stress (OS), thereby improving experimental pulmonary arterial hypertension (PAH). Allicin (16 mg/kg) was administered to rats with PAH (monocrotaline 60 mg/kg). Allicin encouraged body weight gain and survival rate, and medial wall thickness and the right ventricle (RV) hypertrophy were prevented. Also, angiotensin II concentrations in the lung (0.37 ± 0.01 vs. 0.47 ± 0.06 pmoles/mL, allicin and control, respectively) and plasma (0.57 ± 0.05 vs. 0.75 ± 0.064, allicin and control respectively) and the expressions of angiotensin-converting enzyme II and angiotensin II type 1 receptor in lung tissue were maintained at normal control levels with allicin. In PAH rats treated with allicin, nitric oxide (NO) (31.72 ± 1.22 and 51.4 ± 3.45 pmoles/mL), tetrahydrobiopterin (8.43 ± 0.33 and 10.14 ± 0.70 pmoles/mL), cyclic guanosine monophosphate (5.54 ± 0.42 and 5.64 ± 0.73 pmoles/mL), and Ang-(1-7) (0.88 ± 0.23 and 0.83 ± 0.056 pmoles/mL) concentrations increased in lung tissue and plasma, respectively. In contrast, dihydrobiopterin increase was prevented in both lung tissue and plasma (5.75 ± 0.3 and 5.64 ± 0.73 pmoles/mL); meanwhile, phosphodiesterase-5 was maintained at normal levels in lung tissue. OS in PAH was prevented with allicin through the increased expression of Nrf2 in the lung. Allicin prevented the lung response to hypoxia, preventing the overexpression of HIF-1α and VEGF. Allicin attenuated the vascular remodeling and RV hypertrophy in PAH through its effects on NO-dependent vasodilation, modulation of RAS, and amelioration of OS. Also, these effects could be associated with the modulation of HIF-1α and improved lung oxygenation. The global effects of allicin contribute to preventing endothelial dysfunction, remodeling of the pulmonary arteries, and RV hypertrophy, preventing heart failure, thus favoring survival. Although human studies are needed, the data suggest that, alone or in combination therapy, allicin may be an alternative in treating PAH if we consider that, similarly to current treatments, it improves lung vasodilation and increase survival. Allicin may be considered an option when there is a lack of efficacy, and where drug intolerance is observed, to enhance the efficacy of drugs, or when more than one pathogenic mechanism must be addressed. Full article
(This article belongs to the Special Issue Molecular Mechanisms, Pathogenesis, and Novel Therapeutic Strategies in Cardiovascular Disease)
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19 pages, 1668 KiB  
Article
Dysregulations of Key Regulators of Angiogenesis and Inflammation in Abdominal Aortic Aneurysm
by Daniel Zalewski, Paulina Chmiel, Przemysław Kołodziej, Grzegorz Borowski, Marcin Feldo, Janusz Kocki and Anna Bogucka-Kocka
Int. J. Mol. Sci. 2023, 24(15), 12087; https://doi.org/10.3390/ijms241512087 - 28 Jul 2023
Cited by 3 | Viewed by 972
Abstract
Abdominal aortic aneurysm (AAA) is a chronic vascular disease caused by localized weakening and broadening of the abdominal aorta. AAA is a clearly underdiagnosed disease and is burdened with a high mortality rate (65–85%) from AAA rupture. Studies indicate that abnormal regulation of [...] Read more.
Abdominal aortic aneurysm (AAA) is a chronic vascular disease caused by localized weakening and broadening of the abdominal aorta. AAA is a clearly underdiagnosed disease and is burdened with a high mortality rate (65–85%) from AAA rupture. Studies indicate that abnormal regulation of angiogenesis and inflammation contributes to progression and onset of this disease; however, dysregulations in the molecular pathways associated with this disease are not yet fully explained. Therefore, in our study, we aimed to identify dysregulations in the key regulators of angiogenesis and inflammation in patients with AAA in peripheral blood mononuclear cells (using qPCR) and plasma samples (using ELISA). Expression levels of ANGPT1, CXCL8, PDGFA, TGFB1, VEGFB, and VEGFC and plasma levels of TGF-alpha, TGF-beta 1, VEGF-A, and VEGF-C were found to be significantly altered in the AAA group compared to the control subjects without AAA. Associations between analyzed factors and risk factors or biochemical parameters were also explored. Any of the analyzed factors was associated with the size of the aneurysm. The presented study identified dysregulations in key angiogenesis- and inflammation-related factors potentially involved in AAA formation, giving new insight into the molecular pathways involved in the development of this disease and providing candidates for biomarkers that could serve as diagnostic or therapeutic targets. Full article
(This article belongs to the Special Issue Molecular Mechanisms, Pathogenesis, and Novel Therapeutic Strategies in Cardiovascular Disease)
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