ijms-logo

Journal Browser

Journal Browser

Ischemic Heart Disease: From Bench to Bedside

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (30 November 2017) | Viewed by 26037

Special Issue Editors

Department of Clinical, Internal, Anesthesiology and Cardiovascular Sciences, Sapienza University of Rome, 00161 Rome, Italy
Interests: heart failure; acute coronary syndrome; pulmonary hypertension; coronary microvascular dysfuntion; coronary artery disease
Special Issues, Collections and Topics in MDPI journals
Department of Integrative Medical Sciences, Northeast Ohio Medical University, Rootstown, OH, USA
Interests: regulatory mechanisms in coronary microcirculation; coronary angiogenesis and arteriogenesis; non-linear behavior of biological systems; mechanosensitive gene expression and signal transduction; redox regulation of ion channel function
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Ischemic heart disease (IHD) is a common disease that, globally, represents an important problem for individuals and healthcare resources. The global problems that IHD causes is not a recent event insofar as the burdens caused by IHD have been known for decades—and researched for nearly the same period of time. For these reasons, an enhanced understanding of its pathophysiology is needed. By convention, IHD is associated with the presence of an atherosclerotic plaque that is able to limit the flow in large-medium sized coronary arteries. Nevertheless, several findings suggest a more complex pathophysiology of IHD. At this time, there is no well-defined assessment of myocardial ischemia pathophysiology. To better examine this complicated disease and to provide evidences and perspective, this Special Issue of IJMS is interested in articles that provide insights into the pathophysiology of IHD. In particular, this Special Issue will focus on researches on all the pathophysiological aspects of IHD, ranging from coronary artery disease (CAD) to coronary microvascular disease (CMD). In fact, IHD is a complex and multifaceted syndrome and its pathophysiology includes different pieces of a single puzzle, including factors as atherosclerosis, inflammation, plaque activation, vasospasm, as well as microcirculation dysfunction raised by abnormalities in endothelium, mitochondria, extravascular forces, redox-signaling, ion channels, myocardium-blood flow cross-talk mismatch, and so on. Specifically, original articles reporting completely new results or reviews of current literature on these aspects of the disease will be taking into account. The Special Issue “Ischemic Heart Disease: From Bench to Bedside” aims to focus on both basic science and translational research, as well as clinical evidence in order to have a more complete comprehension of the pathophysiology of IHD, considering all aspects of this complex puzzle.

Prof. Dr. Francesco Fedele
Prof. Dr. William Chilian
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. 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

  • Coronary artery disease
  • Microvascular dysfunction
  • Myocardial ischemia
  • Myocardial infarction
  • Acute coronary syndrome

Published Papers (3 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Jump to: Review

1660 KiB  
Article
Indoleamine 2,3-Dioxygenase (IDO) Enzyme Links Innate Immunity and Altered T-Cell Differentiation in Non-ST Segment Elevation Acute Coronary Syndrome
by Chiara Zara, Anna Severino, Davide Flego, Aureliano Ruggio, Daniela Pedicino, Ada Francesca Giglio, Francesco Trotta, Claudia Lucci, Domenico D’Amario, Ramona Vinci, Eugenia Pisano, Giulio La Rosa, Luigi Marzio Biasucci, Filippo Crea and Giovanna Liuzzo
Int. J. Mol. Sci. 2018, 19(1), 63; https://doi.org/10.3390/ijms19010063 - 26 Dec 2017
Cited by 8 | Viewed by 4714
Abstract
Atherosclerosis is a chronic inflammatory disease characterized by a complex interplay between innate and adaptive immunity. Dendritic cells (DCs) play a key role in T-cell activation and regulation by promoting a tolerogenic environment through the expression of the immunosuppressive enzyme indoleamine 2,3-dioxygenase (IDO), [...] Read more.
Atherosclerosis is a chronic inflammatory disease characterized by a complex interplay between innate and adaptive immunity. Dendritic cells (DCs) play a key role in T-cell activation and regulation by promoting a tolerogenic environment through the expression of the immunosuppressive enzyme indoleamine 2,3-dioxygenase (IDO), an intracellular enzyme involved in tryptophan catabolism. IDO expression and activity was analyzed in monocytes derived DCs (MDDCs) from non-ST segment elevation myocardial infarction (NSTEMI) patients, stable angina (SA) patients and healthy controls (HC) by real-time quantitative polymerase chain reaction (RT-qPCR) before and after in vitro maturation with lipopolysaccharide (LPS). The amount of tryptophan catabolite; kynurenine; was evaluated in the culture supernatants of mature-MDDCs by ELISA assay. Autologous mixed lymphocyte reaction (MLR) between mature-MDDCs and naïve T-cells was carried out to study the differentiation towards T-helper 1 (Th1) and induced regulatory T-cells (iTreg). Analysis of IDO mRNA transcripts in mature-MDDCs revealed a significant reduction in cells isolated from NSTEMI (625.0 ± 128.2; mean ± SEM) as compared with those from SA (958.5 ± 218.3; p = 0.041) and from HC (1183.6 ± 231.6; p = 0.034). Furthermore; the concentration of kynurenine was lower in NSTEMI patients (2.78 ± 0.2) and SA (2.98 ± 0.25) as compared with HC (5.1 ± 0.69 ng/mL; p = 0.002 and p = 0.016; respectively). When IDO-competent mature-MDDCs were co-cultured with allogeneic naïve T-cells, the ratio between the percentage of generated Th1 and iTreg was higher in NSTEMI (4.4 ± 2.9) than in SA (1.8 ± 0.6; p = 0.056) and HC (0.9 ± 0.3; p = 0.008). In NSTEMI, the tolerogenic mechanism of the immune response related to IDO production by activated MDDCs is altered, supporting their role in T-cell dysregulation. Full article
(This article belongs to the Special Issue Ischemic Heart Disease: From Bench to Bedside)
Show Figures

Figure 1

2239 KiB  
Article
Intracellular Renin Inhibits Mitochondrial Permeability Transition Pore via Activated Mitochondrial Extracellular Signal-Regulated Kinase (ERK) 1/2 during Ischemia in Diabetic Hearts
by Terumori Satoh, Masao Saotome, Hideki Katoh, Daishi Nonaka, Prottoy Hasan, Hideharu Hayashi and Yuichiro Maekawa
Int. J. Mol. Sci. 2018, 19(1), 55; https://doi.org/10.3390/ijms19010055 - 25 Dec 2017
Cited by 4 | Viewed by 3730
Abstract
Although beneficial effects of non-secreting intracellular renin (ns-renin) against ischemia have been reported, the precise mechanism remains unclear. In this study, we investigated the roles of ns-renin and mitochondrial extracellular signal-related kinase (ERK) 1/2 on mitochondrial permeability transition pore (mPTP) opening during ischemia [...] Read more.
Although beneficial effects of non-secreting intracellular renin (ns-renin) against ischemia have been reported, the precise mechanism remains unclear. In this study, we investigated the roles of ns-renin and mitochondrial extracellular signal-related kinase (ERK) 1/2 on mitochondrial permeability transition pore (mPTP) opening during ischemia in diabetes mellitus (DM) hearts. When isolated hearts from Wistar rats (non-DM hearts) and Goto-Kakizaki rats (DM hearts) were subjected to ischemia for 70 min by left anterior descending coronary artery ligation, DM hearts exhibited higher left ventricular (LV) developed pressure and lower LV end-diastolic pressure than non-DM hearts, suggesting ischemic resistance. In addition, DM hearts showed increased intracellular renin (int-renin, including secreting and non-secreting renin) in the ischemic area, and a direct renin inhibitor (DRI; aliskiren) attenuated ischemic resistance in DM hearts. ERK1/2 was significantly phosphorylated after ischemia in both whole cell and mitochondrial fractions in DM hearts. In isolated mitochondria from DM hearts, rat recombinant renin (r-renin) significantly phosphorylated mitochondrial ERK1/2, and hyperpolarized mitochondrial membrane potential (ΔΨm) in a U0126 (an inhibitor of mitogen-activated protein kinases/ERK kinases)-sensitive manner. R-renin also attenuated atractyloside (Atr, an mPTP opener)-induced ΔΨm depolarization and Atr-induced mitochondrial swelling in an U0126-sensitive manner in isolated mitochondria from DM hearts. Furthermore, U0126 attenuated ischemic resistance in DM hearts, whereas it did not alter the hemodynamics in non-DM hearts. Our results suggest that the increased int-renin during ischemia may inhibit mPTP opening through activation of mitochondrial ERK1/2, which may be involved in ischemic resistance in DM hearts. Full article
(This article belongs to the Special Issue Ischemic Heart Disease: From Bench to Bedside)
Show Figures

Figure 1

Review

Jump to: Research

18 pages, 997 KiB  
Review
Recent Advances in Treatment of Coronary Artery Disease: Role of Science and Technology
by Eswar Kandaswamy and Li Zuo
Int. J. Mol. Sci. 2018, 19(2), 424; https://doi.org/10.3390/ijms19020424 - 31 Jan 2018
Cited by 82 | Viewed by 17128
Abstract
Coronary artery disease (CAD) is one of the most common causes of death worldwide. In the last decade, significant advancements in CAD treatment have been made. The existing treatment is medical, surgical or a combination of both depending on the extent, severity and [...] Read more.
Coronary artery disease (CAD) is one of the most common causes of death worldwide. In the last decade, significant advancements in CAD treatment have been made. The existing treatment is medical, surgical or a combination of both depending on the extent, severity and clinical presentation of CAD. The collaboration between different science disciplines such as biotechnology and tissue engineering has led to the development of novel therapeutic strategies such as stem cells, nanotechnology, robotic surgery and other advancements (3-D printing and drugs). These treatment modalities show promising effects in managing CAD and associated conditions. Research on stem cells focuses on studying the potential for cardiac regeneration, while nanotechnology research investigates nano-drug delivery and percutaneous coronary interventions including stent modifications and coatings. This article aims to provide an update on the literature (in vitro, translational, animal and clinical) related to these novel strategies and to elucidate the rationale behind their potential treatment of CAD. Through the extensive and continued efforts of researchers and clinicians worldwide, these novel strategies hold the promise to be effective alternatives to existing treatment modalities. Full article
(This article belongs to the Special Issue Ischemic Heart Disease: From Bench to Bedside)
Show Figures

Figure 1

Back to TopTop