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Heart Disease and Its Complications: From Molecular Mechanisms to Therapy
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Heart Disease and Its Complications: From Molecular Mechanisms to Therapy

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 (15 July 2024) | Viewed by 1669

Special Issue Editor

Dr. Chin-Feng Tsai

E-Mail Website
Guest Editor
School of Medicine, Chung Shan Medical University Division of Cardiology, Chung Shan Medical University Hospital, Taichung City, Taiwan
Interests: arrhythmia; electrophysiology; ablation and device therapy; cardiac fibrosis; signal pathway; atherosclerosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Despite the progress in pharmacotherapy, interventional cardiology and surgery, cardiovascular diseases remain the leading cause of death worldwide and pose a great socioeconomic burden to the society all over the world. Due to the complexity of the etiology and the clinical manifestation, the diagnosis and treatment of the cardiovascular disease are still unmet medical needs. Besides, the molecular and cellular mechanisms underlying various cardiovascular diseases are not completely understood. Therefore, understanding the mechanisms underlying the pathogenesis of various cardiovascular disorders will confer a great opportunity to delineate diagnostic tools and therapeutic interventions for the early detection and effective therapy of cardiovascular diseases.

This Special Issue will focus on cutting-edge research that provides solutions to the challenges of diagnosing and treating patients with cardiovascular diseases. We are looking for original research articles, communications and comprehensive reviews. Articles that investigate novel molecular mechanisms from the perspective of diagnosis/therapy are especially welcome.

Dr. Chin-Feng Tsai
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

  • cardiovascular disease
  • atherosclerosis
  • arrhythmia
  • heart failure
  • signal pathway
  • molecular/cellular mechanism
  • pathogenesis

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Published Papers (2 papers)

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Research

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19 pages, 3627 KiB  
Article
Chronic Partial Sleep Deprivation Increased the Incidence of Atrial Fibrillation by Promoting Pulmonary Vein and Atrial Arrhythmogenesis in a Rodent Model
by Shuen-Hsin Liu, Fong-Jhih Lin, Yu-Hsun Kao, Pao-Huan Chen, Yung-Kuo Lin, Yen-Yu Lu, Yao-Chang Chen and Yi-Jen Chen
Int. J. Mol. Sci. 2024, 25(14), 7619; https://doi.org/10.3390/ijms25147619 - 11 Jul 2024
Viewed by 672
Abstract
Sleep deprivation (SD) is a recognized risk factor for atrial fibrillation (AF), yet the precise molecular and electrophysiological mechanisms behind SD-induced AF are unclear. This study explores the electrical and structural changes that contribute to AF in chronic partial SD. We induced chronic [...] Read more.
Sleep deprivation (SD) is a recognized risk factor for atrial fibrillation (AF), yet the precise molecular and electrophysiological mechanisms behind SD-induced AF are unclear. This study explores the electrical and structural changes that contribute to AF in chronic partial SD. We induced chronic partial SD in Wistar rats using a modified multiple-platform method. Echocardiography demonstrated impaired systolic and diastolic function in the left ventricle (LV) of the SD rats. The SD rats exhibited an elevated heart rate and a higher low-frequency to high-frequency ratio in a heart-rate variability analysis. Rapid transesophageal atrial pacing led to a higher incidence of AF and longer mean AF durations in the SD rats. Conventional microelectrode recordings showed accelerated pulmonary vein (PV) spontaneous activity in SD rats, along with a heightened occurrence of delayed after-depolarizations in the PV and left atrium (LA) induced by tachypacing and isoproterenol. A Western blot analysis showed reduced expression of G protein-coupled receptor kinase 2 (GRK2) in the LA of the SD rats. Chronic partial SD impairs LV function, promotes AF genesis, and increases PV and LA arrhythmogenesis, potentially attributed to sympathetic overactivity and reduced GRK2 expression. Targeting GRK2 signaling may offer promising therapeutic avenues for managing chronic partial SD-induced AF. Future investigations are mandatory to investigate the dose–response relationship between SD and AF genesis. Full article
(This article belongs to the Special Issue Heart Disease and Its Complications: From Molecular Mechanisms to Therapy)
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Review

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27 pages, 3011 KiB  
Review
The Future of Kawasaki Disease Diagnosis: Liquid Biopsy May Hold the Key
by Kasturi Markandran, Kristine Nicole Mendoza Clemente, Elena Tan, Karan Attal, Qiao Zhi Chee, Christine Cheung and Ching Kit Chen
Int. J. Mol. Sci. 2024, 25(15), 8062; https://doi.org/10.3390/ijms25158062 - 24 Jul 2024
Viewed by 701
Abstract
Kawasaki disease (KD) is a febrile illness characterised by systemic inflammation of small- and medium-sized blood vessels, which commonly occurs in young children. Although self-limiting, there is a risk of developing coronary artery lesions as the disease progresses, with delay in diagnosis and [...] Read more.
Kawasaki disease (KD) is a febrile illness characterised by systemic inflammation of small- and medium-sized blood vessels, which commonly occurs in young children. Although self-limiting, there is a risk of developing coronary artery lesions as the disease progresses, with delay in diagnosis and treatment. Unfortunately, the diagnosis of KD continues to remain a clinical dilemma. Thus, this article not only summarises the key research gaps associated with KD, but also evaluates the possibility of using circulating endothelial injury biomarkers, such as circulating endothelial cells, endothelial microparticles and vascular endothelial cell-free DNA, as diagnostic and prognostic tools for KD: a “liquid biopsy” approach. The challenges of translating liquid biopsies to use in KD and the opportunities for improvement in its diagnosis and management that such translation may provide are discussed. The use of endothelial damage markers, which are easily obtained via blood collection, as diagnostic tools is promising, and we hope this will be translated to clinical applications in the near future. Full article
(This article belongs to the Special Issue Heart Disease and Its Complications: From Molecular Mechanisms to Therapy)
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