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Molecular Mechanism and Pathogenesis of Cardiac Disease
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Molecular Mechanism and Pathogenesis of Cardiac 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: 20 January 2026 | Viewed by 2454

Special Issue Editor

Dr. Yu-Hsun Kao

E-Mail Website
Guest Editor
Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan
Interests: cellular metabolism in cardiac pathophysiology; epigenetic regulation of cardiac pathophysiology; regulation of cardiac fibrosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The understanding of cardiac diseases has significantly advanced with the identification of the molecular regulatory processes underlying their pathophysiology. Epigenetic mechanisms, including non-coding RNA, histone modification, and DNA methylation, play pivotal roles in connecting genetic predispositions with environmental influences in order to modulate gene expression and protein functions in cardiac diseases. Additionally, ER stress and inflammasomes contribute to the inflammatory processes that drive the onset and progression of cardiac diseases. Mitochondria, as essential regulators of cardiac metabolism, biosynthesis, redox balance, calcium homeostasis, and cell death, are a key area of interest for investigating the molecular signaling pathways leading to mitochondrial dysfunction.

In recent years, significant progress has been made in developing therapeutic strategies aimed at targeting these molecular pathways. Advances in drug development, gene therapy, and precision medicine offer promising avenues for improving the treatment and management of cardiac diseases.

The Special Issue, entitled “Molecular Mechanism and Pathogenesis of Cardiac Disease”, aims to provide a comprehensive research platform for the latest original and review articles. We invite contributions that explore molecular biological studies related to the regulation of cardiac diseases, elucidate the mechanisms of therapeutic drugs, and present advancements in treatment strategies designed to enhance cardiac health outcomes.

Dr. Yu-Hsun Kao
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 diseases
  • cardiac metabolidm
  • epigenetics
  • ER stress
  • mitochondrial dysfunction
  • molecular mechanisms
  • therapeutic targets
 

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Published Papers (2 papers)

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Research

16 pages, 2977 KiB  
Article
PCSK9 Enhances Cardiac Fibrogenesis via the Activation of Toll-like Receptor and NLRP3 Inflammasome Signaling
by Cheng-Chih Chung, Yu-Hsun Kao, Yao-Chang Chen, Yung-Kuo Lin, Satoshi Higa, Kai-Cheng Hsu and Yi-Jen Chen
Int. J. Mol. Sci. 2025, 26(5), 1921; https://doi.org/10.3390/ijms26051921 - 23 Feb 2025
Viewed by 1013
Abstract
Proprotein convertase subtilisin/kexin type 9 (PCSK9) has emerged as a novel target for reducing low-density lipoprotein cholesterol. PCSK9 activates the atherosclerosis process through pro-inflammation signaling. Furthermore, the serum level of PCSK9 is positively correlated with mortality in patients with heart failure (HF). Cardiac [...] Read more.
Proprotein convertase subtilisin/kexin type 9 (PCSK9) has emerged as a novel target for reducing low-density lipoprotein cholesterol. PCSK9 activates the atherosclerosis process through pro-inflammation signaling. Furthermore, the serum level of PCSK9 is positively correlated with mortality in patients with heart failure (HF). Cardiac fibrosis plays a crucial role in the pathophysiology of HF. In this study, we intended to examine whether PCSK9 can increase fibroblast activities and explore what its underlying mechanisms are. Migration, proliferation analyses, and Western blotting were used on human cardiac fibroblasts with and without PCSK9. Alirocumab (a PCSK9 inhibitor, 10 mg/kg/week intra-peritoneally for 28 consecutive days) was treated in isoproterenol (100 mg/kg, subcutaneous injection)-induced HF rats. PCSK9 (50, 100 ng/mL) increased proliferation, myofibroblast differentiation capability, and collagen type I production. Compared with control cells, PCSK9 (100 ng/mL)-treated cardiac fibroblasts showed higher nucleotide-binding domain (NOD)-like receptor protein 3 (NLRP3), interleukin (IL)-1, myofibroblast differentiation, and collagen production capabilities, which were attenuated by MCC950 (an NLRP3 inhibitor, 100 μmol/L). PCSK9 upregulated Myd88 and NF-κB signaling, which were reduced by TAK242 (a toll-like receptor (TLR) 4 inhibitor, 10 μmol/L). Moreover, alirocumab significantly improved left ventricular systolic function and attenuated fibrosis in HF rats. In conclusion, PCSK9 upregulates NLRP3 signaling and the profibrotic activities of cardiac fibroblasts through the activation of TLR4/Myd88/NF-κB signaling. Full article
(This article belongs to the Special Issue Molecular Mechanism and Pathogenesis of Cardiac Disease)
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15 pages, 5489 KiB  
Article
Lethal Arrhythmogenic Role of Left Ventricular Myocardial Interstitial Fibrosis in Apolipoprotein E/Low-Density Lipoprotein Receptor Double-Knockout Mice with Metabolic Dysfunction-Associated Steatohepatitis
by Jinyao Liu, Yumiko Oba, Yosuke Kondo, Ryo Nakaki and Seiko Yamano
Int. J. Mol. Sci. 2025, 26(1), 144; https://doi.org/10.3390/ijms26010144 - 27 Dec 2024
Viewed by 878
Abstract
The combination of alcohol and a low-carbohydrate, high-protein, high-fat atherogenic diet (AD) increases the risk of lethal arrhythmias in apolipoprotein E/low-density lipoprotein receptor double-knockout (AL) mice with metabolic dysfunction-associated steatotic liver disease (MASLD). This study investigates whether left ventricular (LV) myocardial interstitial fibrosis [...] Read more.
The combination of alcohol and a low-carbohydrate, high-protein, high-fat atherogenic diet (AD) increases the risk of lethal arrhythmias in apolipoprotein E/low-density lipoprotein receptor double-knockout (AL) mice with metabolic dysfunction-associated steatotic liver disease (MASLD). This study investigates whether left ventricular (LV) myocardial interstitial fibrosis (MIF), formed during the progression of metabolic dysfunction-associated steatohepatitis (MASH), contributes to this increased risk. Male AL mice were fed an AD with or without ethanol for 16 weeks, while age-matched AL and wild-type mice served as controls. Liver and heart tissues were analyzed, and susceptibility to lethal arrhythmias was assessed through histopathology, fluorescence immunohistochemistry, RNA-Seq, RT-PCR, and lethal arrhythmia-evoked test. Ethanol combined with an AD significantly induced LV MIF in MASH-affected AL mice, as shown by increased fibrosis-related gene expression, Sirius-Red staining, and elevated collagen 1a1 and 3a1 mRNA levels, alongside a higher incidence of lethal arrhythmias. Cardiac myofibroblasts exhibited sympathetic activation and produced elevated levels of fibrosis-promoting factors. This study highlights the role of cardiac myofibroblasts in LV MIF, contributing to an increased incidence of lethal arrhythmias in MASH-affected AL mice fed ethanol and AD, even after the alcohol was fully metabolized on the day of consumption. Full article
(This article belongs to the Special Issue Molecular Mechanism and Pathogenesis of Cardiac Disease)
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