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Molecular Mechanisms and Pathogenesis of Cardiac Diseases
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Molecular Mechanisms and Pathogenesis of Cardiac Diseases

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 (30 September 2023) | Viewed by 2291

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,

Emerging evidence has suggested molecular regulating mechanisms play vital roles in pathophysiology of cardiac diseases. Epigenetic mechanisms including non-coding RNA, histone modification, and DNA methylation are crucial connectors to genetics and environmental factors to modify gene expression and protein functions in cardiac diseases. ER stress and inflammasome are implicated in inflammatory processes and also play critical roles in the onset and progression of cardiac diseases. Besides, the mitochondria are central regulators in cardiac metabolism, biosynthesis, redox balance, calcium homeostasis, and cell death. Therefore, the pathological molecular signalling pathways that lead to mitochondrial dysfunction are also much considered in cardiac diseases.

The Special Issue, entitled "Molecular Mechanisms and Pathogenesis of Cardiac Diseases", aims to provide a research platform for the collection of the latest original and review articles covering molecular biological studies of factors related to the control of cardiac diseases and action mechanisms of therapeutic drugs that are targeted at them.

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
  • epigenetic regulator
  • inflammasome
  • mitochondrial dysfunction
  • molecular mechanisms

Published Papers (1 paper)

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Research

17 pages, 2514 KiB  
Article
DAMPs Released from Proinflammatory Macrophages Induce Inflammation in Cardiomyocytes via Activation of TLR4 and TNFR
by Carolina Neu, Yvonne Thiele, Fabienne Horr, Christian Beckers, Nadine Frank, Gernot Marx, Lukas Martin, Sandra Kraemer and Elisabeth Zechendorf
Int. J. Mol. Sci. 2022, 23(24), 15522; https://doi.org/10.3390/ijms232415522 - 8 Dec 2022
Cited by 7 | Viewed by 1965
Abstract
Cardiac dysfunction is a life-threatening complication in sepsis. Upon infection and cardiac stress, the cardiac macrophage population expands. Recruited macrophages exhibit a predominantly proinflammatory phenotype and release danger-associated molecular patterns (DAMPs) that contribute to cardiac dysfunction. However, the underlying pathomechanisms are highly complex [...] Read more.
Cardiac dysfunction is a life-threatening complication in sepsis. Upon infection and cardiac stress, the cardiac macrophage population expands. Recruited macrophages exhibit a predominantly proinflammatory phenotype and release danger-associated molecular patterns (DAMPs) that contribute to cardiac dysfunction. However, the underlying pathomechanisms are highly complex and not fully understood. Here, we utilized an indirect macrophage–cardiomyocyte co-culture model to study the effects of proinflammatory macrophages on the activation of different cardiac receptors (TLR3, TLR4, and TNFR) and their role in cardiac inflammation and caspase-3/7 activation. The stimulation of cardiomyocytes with conditioned medium of LPS-stimulated macrophages resulted in elevated IL-6 protein concentrations and relative IL-6 and TNFα mRNA levels. Conditioned medium from LPS-stimulated macrophages also induced NFκB translocation and increased caspase-3/7 activation in cardiomyocytes. Analyzing the role of different cardiac receptors, we found that TLR4 and TNFR inhibition reduces cardiac inflammation and that the inhibition of TNFR prevents NFκB translocation into the nuclei of cardiomyocytes, induced by exposure to conditioned medium of proinflammatory macrophages. Moreover, we demonstrated that TLR3 inhibition reduces macrophage-mediated caspase-3/7 activation. Our results suggest that the immune response of macrophages under inflammatory conditions leads to the release of DAMPs, such as eRNA and cytokines, which in turn induce cardiomyocyte dysfunction. Thus, the data obtained in this study contribute to a better understanding of the pathophysiological mechanisms of cardiac dysfunction. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pathogenesis of Cardiac Diseases)
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