Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
9.4
4.8
Journals
Biomolecules
Special Issues
Aortic Aneurysm and Dissection: Heterogeneity and Molecular Mechanisms
share announcement

Aortic Aneurysm and Dissection: Heterogeneity and Molecular Mechanisms

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (10 July 2022) | Viewed by 44737

Special Issue Editors

Dr. Hong S. Lu

E-Mail Website
Guest Editor
Department of Physiology, Saha Cardiovascular Research Center, College of Medicine, University of Kentucky, Lexington, KY 40536-0509, USA
Interests: renin–angiotensin system; angiotensinogen; megalin; kidney; atherosclerosis; aortic aneurysm and aortic dissection; mouse
Dr. Congqing Wu

E-Mail Website
Guest Editor
Department of Surgery, Saha Cardiovascular Research Center, College of Medicine, University of Kentucky, Lexington, KY 40536-0509, USA
Interests: atherosclerosis; aortic aneurysm and dissection; inflammation; pyroptosis; macrophages
Dr. Hisashi Sawada

E-Mail Website
Guest Editor
Department of Physiology, Saha Cardiovascular Research Center, College of Medicine, University of Kentucky, Lexington, KY 40536-0509, USA
Interests: aortic aneurysm and dissection; smooth muscle cells; LRP1; TGF beta; embryonic origins

Special Issue Information

Dear Colleagues,

We are delighted to announce a Special Issue on “Aortic Aneurysm and Dissection: Heterogeneity and Molecular Mechanisms”.

Aortic aneurysm and dissection are devastating diseases that have high risk for aortic rupture, leading to uncontrolled bleeding and death. Aortic aneurysm and dissection have complex pathophysiological features. Despite progress in our understanding of potential molecular mechanisms, there are still many unanswered questions and conflicting findings requiring clarification. Improved understandings of the pathological heterogeneity, subcellular mechanisms, and regulatory networks triggering the disease development and progression are essential for exploring potential therapeutic targets. This Topical Collection of Biomolecules aims to highlight the pathological heterogeneity and molecular mechanisms of aortic aneurysm and dissection. Studies addressing the diversity and function of pathogenesis in arteries derived from the aorta are also of interest.

Dr. Hong S. Lu
Dr. Congqing Wu
Dr. Hisashi Sawada
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. Biomolecules 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 2700 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

  • aortic aneurysms
  • aortic dissection
  • inflammation
  • smooth muscle cells
  • elastin

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

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

Published Papers (12 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Editorial

Jump to: Research, Review, Other

3 pages, 184 KiB  
Editorial
Aortic Aneurysm and Dissection: Heterogeneity and Molecular Mechanisms
by Hong S. Lu, Hisashi Sawada and Congqing Wu
Biomolecules 2022, 12(10), 1536; https://doi.org/10.3390/biom12101536 - 21 Oct 2022
Cited by 1 | Viewed by 1446
Abstract
Aortic aneurysms and dissections (AAD) are devastating aortic diseases with high risks for aortic rupture, leading to uncontrolled bleeding and death [...] Full article
(This article belongs to the Special Issue Aortic Aneurysm and Dissection: Heterogeneity and Molecular Mechanisms)

Research

Jump to: Editorial, Review, Other

14 pages, 1874 KiB  
Article
Edaravone Attenuated Angiotensin II-Induced Atherosclerosis and Abdominal Aortic Aneurysms in Apolipoprotein E-Deficient Mice
by Haruhito A. Uchida, Tetsuharu Takatsuka, Yoshiko Hada, Ryoko Umebayashi, Hidemi Takeuchi, Kenichi Shikata, Venkateswaran Subramanian, Alan Daugherty and Jun Wada
Biomolecules 2022, 12(8), 1117; https://doi.org/10.3390/biom12081117 - 14 Aug 2022
Cited by 4 | Viewed by 2694
Abstract
Background: The aim of the study was to define whether edaravone, a free-radical scavenger, influenced angiotensin II (AngII)-induced atherosclerosis and abdominal aortic aneurysms (AAAs) formation. Methods: Male apolipoprotein E-deficient mice (8–12 weeks old) were fed with a normal diet for 5 weeks. Either [...] Read more.
Background: The aim of the study was to define whether edaravone, a free-radical scavenger, influenced angiotensin II (AngII)-induced atherosclerosis and abdominal aortic aneurysms (AAAs) formation. Methods: Male apolipoprotein E-deficient mice (8–12 weeks old) were fed with a normal diet for 5 weeks. Either edaravone (10 mg/kg/day) or vehicle was injected intraperitoneally for 5 weeks. After 1 week of injections, mice were infused subcutaneously with either AngII (1000 ng/kg/min, n = 16–17 per group) or saline (n = 5 per group) by osmotic minipumps for 4 weeks. Results: AngII increased systolic blood pressure equivalently in mice administered with either edaravone or saline. Edaravone had no effect on plasma total cholesterol concentrations and body weights. AngII infusion significantly increased ex vivo maximal diameters of abdominal aortas and en face atherosclerosis but was significantly attenuated by edaravone administration. Edaravone also reduced the incidence of AngII-induced AAAs. In addition, edaravone diminished AngII-induced aortic MMP-2 activation. Quantitative RT-PCR revealed that edaravone ameliorated mRNA abundance of aortic MCP-1 and IL-1β. Immunostaining demonstrated that edaravone attenuated oxidative stress and macrophage accumulation in the aorta. Furthermore, edaravone administration suppressed thioglycolate-induced mice peritoneal macrophages (MPMs) accumulation and mRNA abundance of MCP-1 in MPMs in male apolipoprotein E-deficient mice. In vitro, edaravone reduced LPS-induced mRNA abundance of MCP-1 in MPMs. Conclusions: Edaravone attenuated AngII-induced AAAs and atherosclerosis in male apolipoprotein E-deficient mice via anti-oxidative action and anti-inflammatory effect. Full article
(This article belongs to the Special Issue Aortic Aneurysm and Dissection: Heterogeneity and Molecular Mechanisms)
►▼ Show Figures

Figure 1

15 pages, 4119 KiB  
Article
No Effect of Hypercholesterolemia on Elastase-Induced Experimental Abdominal Aortic Aneurysm Progression
by Toru Ikezoe, Takahiro Shoji, Jia Guo, Fanru Shen, Hong S. Lu, Alan Daugherty, Masao Nunokawa, Hiroshi Kubota, Masaaki Miyata, Baohui Xu and Ronald L. Dalman
Biomolecules 2021, 11(10), 1434; https://doi.org/10.3390/biom11101434 - 30 Sep 2021
Cited by 17 | Viewed by 3981
Abstract
Objective: Epidemiological studies link hyperlipidemia with increased risk for abdominal aortic aneurysms (AAAs). However, the influence of lipid-lowering drugs statins on prevalence and progression of clinical and experimental AAAs varies between reports, engendering controversy on the association of hyperlipidemia with AAA disease. This [...] Read more.
Objective: Epidemiological studies link hyperlipidemia with increased risk for abdominal aortic aneurysms (AAAs). However, the influence of lipid-lowering drugs statins on prevalence and progression of clinical and experimental AAAs varies between reports, engendering controversy on the association of hyperlipidemia with AAA disease. This study investigated the impact of hypercholesterolemia on elastase-induced experimental AAAs in mice. Methods: Both spontaneous (targeted deletion of apolipoprotein E) and induced mouse hypercholesterolemia models were employed. In male wild type (WT) C57BL/6J mice, hypercholesterolemia was induced via intraperitoneal injection of an adeno-associated virus (AAV) encoding a gain-of-function proprotein convertase subtilisin/kexin type 9 mutation (PCSK9) followed by the administration of a high-fat diet (HFD) (PCSK9+HFD) for two weeks. As normocholesterolemic controls for PCSK9+HFD mice, WT mice were infected with PCSK9 AAV and fed normal chow, or injected with phosphate-buffered saline alone and fed HFD chow. AAAs were induced in all mice by intra-aortic infusion of porcine pancreatic elastase and assessed by ultrasonography and histopathology. Results: In spontaneous hyper- and normo-cholesterolemic male mice, the aortic diameter enlarged at a constant rate from day 3 through day 14 following elastase infusion. AAAs, defined as a more than 50% diameter increase over baseline measurements, formed in all mice. AAA progression was more pronounced in male mice, with or without spontaneous hyperlipidemia. The extent of elastin degradation and smooth muscle cell depletion were similar in spontaneous hyper- (score 3.5 for elastin and 4.0 for smooth muscle) and normo- (both scores 4.0) cholesterolemic male mice. Aortic mural macrophage accumulation was also equivalent between the two groups. No differences were observed in aortic accumulation of CD4+ or CD8+ T cells, B cells, or mural angiogenesis between male spontaneous hyper- and normocholesterolemic mice. Similarly, no influence of spontaneous hypercholesterolemia on characteristic aneurysmal histopathology was noted in female mice. In confirmatory experiments, induced hypercholesterolemia also exerted no appreciable effect on AAA progression and histopathologies. Conclusion: This study demonstrated no recognizable impact of hypercholesterolemia on elastase-induced experimental AAA progression in both spontaneous and induced hypercholesterolemia mouse models. These results add further uncertainty to the controversy surrounding the efficacy of statin therapy in clinical AAA disease. Full article
(This article belongs to the Special Issue Aortic Aneurysm and Dissection: Heterogeneity and Molecular Mechanisms)
►▼ Show Figures

Figure 1

Review

Jump to: Editorial, Research, Other

14 pages, 674 KiB  
Review
Endothelial Dysfunction in the Pathogenesis of Abdominal Aortic Aneurysm
by Elise DeRoo, Amelia Stranz, Huan Yang, Marvin Hsieh, Caitlyn Se and Ting Zhou
Biomolecules 2022, 12(4), 509; https://doi.org/10.3390/biom12040509 - 28 Mar 2022
Cited by 28 | Viewed by 6968
Abstract
Abdominal aortic aneurysm (AAA), defined as a focal dilation of the abdominal aorta beyond 50% of its normal diameter, is a common and potentially life-threatening vascular disease. The molecular and cellular mechanisms underlying AAA pathogenesis remain unclear. Healthy endothelial cells (ECs) play a [...] Read more.
Abdominal aortic aneurysm (AAA), defined as a focal dilation of the abdominal aorta beyond 50% of its normal diameter, is a common and potentially life-threatening vascular disease. The molecular and cellular mechanisms underlying AAA pathogenesis remain unclear. Healthy endothelial cells (ECs) play a critical role in maintaining vascular homeostasis by regulating vascular tone and maintaining an anti-inflammatory, anti-thrombotic local environment. Increasing evidence indicates that endothelial dysfunction is an early pathologic event in AAA formation, contributing to both oxidative stress and inflammation in the degenerating arterial wall. Recent studies utilizing single-cell RNA sequencing revealed heterogeneous EC sub-populations, as determined by their transcriptional profiles, in aortic aneurysm tissue. This review summarizes recent findings, including clinical evidence of endothelial dysfunction in AAA, the impact of biomechanical stress on EC in AAA, the role of endothelial nitric oxide synthase (eNOS) uncoupling in AAA, and EC heterogeneity in AAA. These studies help to improve our understanding of AAA pathogenesis and ultimately may lead to the generation of EC-targeted therapeutics to treat or prevent this deadly disease. Full article
(This article belongs to the Special Issue Aortic Aneurysm and Dissection: Heterogeneity and Molecular Mechanisms)
►▼ Show Figures

Figure 1

14 pages, 1161 KiB  
Review
Imaging Techniques for Aortic Aneurysms and Dissections in Mice: Comparisons of Ex Vivo, In Situ, and Ultrasound Approaches
by Sohei Ito, Hong S. Lu, Alan Daugherty and Hisashi Sawada
Biomolecules 2022, 12(2), 339; https://doi.org/10.3390/biom12020339 - 21 Feb 2022
Cited by 9 | Viewed by 3405
Abstract
Aortic aneurysms and dissections are life-threatening conditions that have a high risk for lethal bleeding and organ malperfusion. Many studies have investigated the molecular basis of these diseases using mouse models. In mice, ex vivo, in situ, and ultrasound imaging are major approaches [...] Read more.
Aortic aneurysms and dissections are life-threatening conditions that have a high risk for lethal bleeding and organ malperfusion. Many studies have investigated the molecular basis of these diseases using mouse models. In mice, ex vivo, in situ, and ultrasound imaging are major approaches to evaluate aortic diameters, a common parameter to determine the severity of aortic aneurysms. However, accurate evaluations of aortic dimensions by these imaging approaches could be challenging due to pathological features of aortic aneurysms. Currently, there is no standardized mode to assess aortic dissections in mice. It is important to understand the characteristics of each approach for reliable evaluation of aortic dilatations. In this review, we summarize imaging techniques used for aortic visualization in recent mouse studies and discuss their pros and cons. We also provide suggestions to facilitate the visualization of mouse aortas. Full article
(This article belongs to the Special Issue Aortic Aneurysm and Dissection: Heterogeneity and Molecular Mechanisms)
►▼ Show Figures

Figure 1

15 pages, 651 KiB  
Review
Targeting Platelet Activation in Abdominal Aortic Aneurysm: Current Knowledge and Perspectives
by Weiliang Sun, Jingang Zheng and Yanxiang Gao
Biomolecules 2022, 12(2), 206; https://doi.org/10.3390/biom12020206 - 25 Jan 2022
Cited by 14 | Viewed by 3960
Abstract
Abdominal aortic aneurysm (AAA) is a potentially fatal vascular disease that involves complex multifactorial hemodynamic, thrombotic, inflammatory, and aortic wall remodeling processes. However, its mechanisms are incompletely understood. It has become increasingly clear that platelets are involved in pathological processes of vascular diseases [...] Read more.
Abdominal aortic aneurysm (AAA) is a potentially fatal vascular disease that involves complex multifactorial hemodynamic, thrombotic, inflammatory, and aortic wall remodeling processes. However, its mechanisms are incompletely understood. It has become increasingly clear that platelets are involved in pathological processes of vascular diseases beyond their role in hemostasis and thrombosis. Platelet activation with membrane receptors and secreted mediators promotes thrombus formation and the accumulation of inflammatory cells, which may play an important role in the development of AAA by destroying the structural integrity and stability of the vessel wall. Turbulent blood flow in aortic aneurysms promotes platelet activation and aggregation. Platelet count and heterogeneity are important predictive, diagnostic, and prognostic indicators of AAA. We summarize the relationship between platelet activation and AAA development and propose future research directions and possible clinical applications. Full article
(This article belongs to the Special Issue Aortic Aneurysm and Dissection: Heterogeneity and Molecular Mechanisms)
►▼ Show Figures

Figure 1

14 pages, 280 KiB  
Review
The Role of Epigenetic Modifications in Abdominal Aortic Aneurysm Pathogenesis
by Kevin Mangum, Katherine Gallagher and Frank M. Davis
Biomolecules 2022, 12(2), 172; https://doi.org/10.3390/biom12020172 - 21 Jan 2022
Cited by 12 | Viewed by 2895
Abstract
Abdominal aortic aneurysm (AAA) is a life-threatening disease associated with high morbidity and mortality in the setting of acute rupture. Recently, advances in surgical and endovascular repair of AAA have been achieved; however, pharmaceutical therapies to prevent AAA expansion and rupture remain lacking. [...] Read more.
Abdominal aortic aneurysm (AAA) is a life-threatening disease associated with high morbidity and mortality in the setting of acute rupture. Recently, advances in surgical and endovascular repair of AAA have been achieved; however, pharmaceutical therapies to prevent AAA expansion and rupture remain lacking. This highlights an ongoing need to improve the understanding the pathological mechanisms that initiate formation, maintain growth, and promote rupture of AAA. Over the past decade, epigenetic modifications, such as DNA methylation, posttranslational histone modifications, and non-coding RNA, have emerged as important regulators of cellular function. Accumulating studies reveal the importance of epigenetic enzymes in the dynamic regulation of key signaling pathways that alter cellular phenotypes and have emerged as major intracellular players in a wide range of biological processes. In this review, we discuss the roles and implications of epigenetic modifications in AAA animal models and their relevance to human AAA pathology. Full article
(This article belongs to the Special Issue Aortic Aneurysm and Dissection: Heterogeneity and Molecular Mechanisms)
10 pages, 1938 KiB  
Review
Pathophysiology and Therapeutics of Thoracic Aortic Aneurysm in Marfan Syndrome
by Keiichi Asano, Anna Cantalupo, Lauriane Sedes and Francesco Ramirez
Biomolecules 2022, 12(1), 128; https://doi.org/10.3390/biom12010128 - 14 Jan 2022
Cited by 18 | Viewed by 5334
Abstract
About 20% of individuals afflicted with thoracic aortic disease have single-gene mutations that predispose the vessel to aneurysm formation and/or acute aortic dissection often without associated syndromic features. One widely studied exception is Marfan syndrome (MFS) in which mutations in the extracellular protein [...] Read more.
About 20% of individuals afflicted with thoracic aortic disease have single-gene mutations that predispose the vessel to aneurysm formation and/or acute aortic dissection often without associated syndromic features. One widely studied exception is Marfan syndrome (MFS) in which mutations in the extracellular protein fibrillin-1 cause additional abnormalities in the heart, eyes, and skeleton. Mouse models of MFS have been instrumental in delineating major cellular and molecular determinants of thoracic aortic disease. In spite of research efforts, translating experimental findings from MFS mice into effective drug therapies for MFS patients remains an unfulfilled promise. Here, we describe a series of studies that have implicated endothelial dysfunction and improper angiotensin II and TGFβ signaling in driving thoracic aortic disease in MFS mice. We also discuss how these investigations have influenced the way we conceptualized possible new therapies to slow down or even halt aneurysm progression in this relatively common connective tissue disorder. Full article
(This article belongs to the Special Issue Aortic Aneurysm and Dissection: Heterogeneity and Molecular Mechanisms)
►▼ Show Figures

Figure 1

Other

6 pages, 1257 KiB  
Commentary
Expression of a PCSK9 Gain-of-Function Mutation in C57BL/6J Mice to Facilitate Angiotensin II-Induced AAAs
by Hisashi Sawada, Alan Daugherty and Hong S. Lu
Biomolecules 2022, 12(7), 915; https://doi.org/10.3390/biom12070915 - 29 Jun 2022
Cited by 4 | Viewed by 2193
Abstract
Angiotensin II (AngII) infusion in mice has been used widely to investigate mechanisms of abdominal aortic aneurysms (AAAs). To achieve a high incidence of AngII-induced AAAs, mice should be hypercholesterolemic. Therefore, either low-density lipoprotein receptor (LDLR) or apolipoprotein E deficiency have been used [...] Read more.
Angiotensin II (AngII) infusion in mice has been used widely to investigate mechanisms of abdominal aortic aneurysms (AAAs). To achieve a high incidence of AngII-induced AAAs, mice should be hypercholesterolemic. Therefore, either low-density lipoprotein receptor (LDLR) or apolipoprotein E deficiency have been used as a hypercholesterolemic background. However, it is a time-consuming and expensive process to generate compound deficient strains that have either an LDLR or apolipoprotein E deficient background. Proprotein convertase subtilisin/kexin type 9 (PCSK9) facilitates the degradation of LDL receptors. Previous studies demonstrated profound increases of plasma cholesterol concentrations after a single intraperitoneal injection of adeno-associated viruses (AAV) expressing a gain-of-function mutation of mouse PCSK9 (AAV.mPCSK9D377Y) in C57BL/6J mice fed a Western diet. Of note, injection of AAV.mPCSK9D377Y augmented AngII-induced AAA formation in C57BL/6J mice that had comparable severity of AAAs to LDLR deficient mice. Thus, AAV.mPCSK9D377Y infection greatly expedites studies on a gene of interest using AngII-induced AAAs. This commentary provides a brief technical guide of this approach and discusses the pros and cons of its use in AAA research. Full article
(This article belongs to the Special Issue Aortic Aneurysm and Dissection: Heterogeneity and Molecular Mechanisms)
►▼ Show Figures

Figure 1

12 pages, 7281 KiB  
Brief Report
Fludrocortisone Induces Aortic Pathologies in Mice
by Dien Ye, Congqing Wu, Hui Chen, Ching-Ling Liang, Deborah A. Howatt, Michael K. Franklin, Jessica J. Moorleghen, Samuel C. Tyagi, Estrellita Uijl, A. H. Jan Danser, Hisashi Sawada, Alan Daugherty and Hong S. Lu
Biomolecules 2022, 12(6), 825; https://doi.org/10.3390/biom12060825 - 13 Jun 2022
Cited by 3 | Viewed by 2620
Abstract
Background and Objective: In an experiment designed to explore the mechanisms of fludrocortisone-induced high blood pressure, we serendipitously observed aortic aneurysms in mice infused with fludrocortisone. The purpose of this study was to investigate whether fludrocortisone induces aortic pathologies in both normocholesterolemic and [...] Read more.
Background and Objective: In an experiment designed to explore the mechanisms of fludrocortisone-induced high blood pressure, we serendipitously observed aortic aneurysms in mice infused with fludrocortisone. The purpose of this study was to investigate whether fludrocortisone induces aortic pathologies in both normocholesterolemic and hypercholesterolemic mice. Methods and Results: Male adult C57BL/6J mice were infused with either vehicle (85% polyethylene glycol 400 (PEG-400) and 15% dimethyl sulfoxide (DMSO); n = 5) or fludrocortisone (12 mg/kg/day dissolved in 85% PEG-400 and 15% DMSO; n = 15) for 28 days. Fludrocortisone-infused mice had higher systolic blood pressure, compared to mice infused with vehicle. Fludrocortisone induced aortic pathologies in 4 of 15 mice with 3 having pathologies in the ascending and aortic arch regions and 1 having pathology in both the ascending and descending thoracic aorta. No pathologies were noted in abdominal aortas. Subsequently, we infused either vehicle (n = 5/group) or fludrocortisone (n = 15/group) into male ApoE −/− mice fed a normal laboratory diet or LDL receptor −/− mice fed either normal or Western diet. Fludrocortisone increased systolic blood pressure, irrespective of mouse strain or diet. In ApoE −/− mice infused with fludrocortisone, 2 of 15 mice had ascending aortic pathologies, but no mice had abdominal aortic pathologies. In LDL receptor −/− mice fed normal diet, 5 had ascending/arch pathologies and 1 had pathologies in the ascending, arch, and suprarenal aortic regions. In LDL receptor −/− mice fed Western diet, 2 died of aortic rupture in either the descending thoracic or abdominal region, and 2 of the 13 survived mice had ascending/arch aortic pathologies. Aortic pathologies included hemorrhage, wall thickening or thinning, or dilation. Only ascending aortic diameter in LDLR −/− mice fed Western diet reached statistical significance, compared to their vehicle. Conclusion: Fludrocortisone induces aortic pathologies independent of hypercholesterolemia. As indicated by the findings in mouse studies, people who are taking or have taken fludrocortisone might have an increased risk of aortic pathologies. Full article
(This article belongs to the Special Issue Aortic Aneurysm and Dissection: Heterogeneity and Molecular Mechanisms)
►▼ Show Figures

Graphical abstract

6 pages, 2772 KiB  
Commentary
Fibrates: A Possible Treatment Option for Patients with Abdominal Aortic Aneurysm?
by Naofumi Amioka and Toru Miyoshi
Biomolecules 2022, 12(1), 74; https://doi.org/10.3390/biom12010074 - 5 Jan 2022
Cited by 5 | Viewed by 4214
Abstract
Abdominal aortic aneurysm (AAA) is a life-threatening disease; however, there is no established treatment for patients with AAA. Fibrates are agonists of peroxisome proliferator-activated receptor alpha (PPARα) that are widely used as therapeutic agents to treat patients with hypertriglyceridemia. They can regulate the [...] Read more.
Abdominal aortic aneurysm (AAA) is a life-threatening disease; however, there is no established treatment for patients with AAA. Fibrates are agonists of peroxisome proliferator-activated receptor alpha (PPARα) that are widely used as therapeutic agents to treat patients with hypertriglyceridemia. They can regulate the pathogenesis of AAA in multiple ways, for example, by exerting anti-inflammatory and anti-oxidative effects and suppressing the expression of matrix metalloproteinases. Previously, basic and clinical studies have evaluated the effects of fenofibrate on AAA. In this paper, we summarize the results of these studies and discuss the problems associated with using fenofibrate as a therapeutic agent for patients with AAA. In addition, we discuss a new perspective on the regulation of AAA by PPARα agonists. Full article
(This article belongs to the Special Issue Aortic Aneurysm and Dissection: Heterogeneity and Molecular Mechanisms)
►▼ Show Figures

Figure 1

13 pages, 1072 KiB  
Perspective
Role of Serum Amyloid A in Abdominal Aortic Aneurysm and Related Cardiovascular Diseases
by Preetha Shridas, Avery C. Patrick and Lisa R. Tannock
Biomolecules 2021, 11(12), 1883; https://doi.org/10.3390/biom11121883 - 15 Dec 2021
Cited by 13 | Viewed by 3427
Abstract
Epidemiological data positively correlate plasma serum amyloid A (SAA) levels with cardiovascular disease severity and mortality. Studies by several investigators have indicated a causal role for SAA in the development of atherosclerosis in animal models. Suppression of SAA attenuates the development of angiotensin [...] Read more.
Epidemiological data positively correlate plasma serum amyloid A (SAA) levels with cardiovascular disease severity and mortality. Studies by several investigators have indicated a causal role for SAA in the development of atherosclerosis in animal models. Suppression of SAA attenuates the development of angiotensin II (AngII)-induced abdominal aortic aneurysm (AAA) formation in mice. Thus, SAA is not just a marker for cardiovascular disease (CVD) development, but it is a key player. However, to consider SAA as a therapeutic target for these diseases, the pathway leading to its involvement needs to be understood. This review provides a brief description of the pathobiological significance of this enigmatic molecule. The purpose of this review is to summarize the data relevant to its role in the development of CVD, the pitfalls in SAA research, and unanswered questions in the field. Full article
(This article belongs to the Special Issue Aortic Aneurysm and Dissection: Heterogeneity and Molecular Mechanisms)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-12
Back to TopTop