ijms-logo

Journal Browser

Journal Browser

Therapeutic Target 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: 31 October 2024 | Viewed by 363

Special Issue Editor


E-Mail Website
Guest Editor
Inha Research Institute for Aerospace Medicine, Inha University, Seohae daero 366, Joong gu, Incheon, Republic of Korea
Interests: otorhinolaryngology-head and neck surgery

Special Issue Information

Dear Colleagues,

Regulated calcium handling in each cardiac cell is essential for optimal electrical and mechanical function of the heart. Abnormalities in calcium handling in the heart are associated with cardiovascular diseases such as heart failure and atrial fibrillation, including arrhythmic cardiomyopathy. The exact role of calcium in the progression of these diseases is a result of complex interactions among many electrophysiological targets and signaling systems, and mechanisms of heart disease development, such as cardiac fibrosis, oxidative stress, and changes in ion channel function, are being widely studied to date. Despite more refined therapeutic targets proposed in recent years, most currently available pharmacological treatments are still limited by incomplete efficacy, side effects, and significant recurrence rates. On this basis, this special issue aims to provide diverse theoretical bases and creative potential therapeutic strategies for the prevention and treatment of cardiac diseases, and to present important therapeutic targets and clinically relevant mechanisms.

Dr. Hyelim Park
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

  • cardiac disease
  • arrhythmia
  • cardiac remodeling
  • therapeutic target

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 (1 paper)

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

Research

11 pages, 1336 KiB  
Article
Therapeutic Potential of Intermittent Hypoxia in Atrial Fibrillation
by Hyewon Park, Bokyeong Park, Kyu-sung Kim, Young Hoon Son, Sung Jin Park, Kichang Lee, Hyelim Park and Junbeom Park
Int. J. Mol. Sci. 2024, 25(20), 11085; https://doi.org/10.3390/ijms252011085 - 15 Oct 2024
Viewed by 222
Abstract
Intermittent hypoxia (IH) has been extensively studied in recent years, demonstrating adverse and beneficial effects on several physiological systems. However, the precise mechanism underlying its cardiac effects on the heart remains unclear. This study aims to explore the effect of treatment on atrial [...] Read more.
Intermittent hypoxia (IH) has been extensively studied in recent years, demonstrating adverse and beneficial effects on several physiological systems. However, the precise mechanism underlying its cardiac effects on the heart remains unclear. This study aims to explore the effect of treatment on atrial fibrillation under IH conditions, providing data that can potentially be used in the treatment of heart disease. An atrial fibrillation (AF) model was induced by injecting monocrotaline (MCT, 60 mg/kg) into rats. The study included 32 rats divided into four groups: Control, Control + IH, AF, and AF + IH. We evaluated molecular changes associated with AF using ELISA and Western blot and performed electrophysiological experiments to evaluate AF. Arrhythmia-related calcium and fibrosis markers were investigated. Phosphorylation levels of CaMKII, Phospholamban, and RyR2 all increased in the AF group but decreased in the IH-exposed group. Additionally, fibrosis marker expressions such as SMA, MMP2, MMP9, and TGF-β increased in the AF group but were significantly downregulated with IH treatment. Connexin 43 and AQP4 expression were restored in the IH-treated group. These findings suggest that IH may prevent AF by downregulating the expression of calcium-handling proteins and fibrosis-associated proteins in an AF-induced rat model. Full article
(This article belongs to the Special Issue Therapeutic Target in Cardiovascular Disease)
Show Figures

Figure 1

Back to TopTop