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Cardiac Diseases: Molecular Mechanisms and Therapeutic Strategies

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

Deadline for manuscript submissions: closed (31 October 2024) | Viewed by 4482

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Guest Editor
Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil
Interests: cellular electrophysiology

Special Issue Information

Dear Colleagues,

Ion channels, membrane proteins that facilitate the passage of various ions across cell membranes, play a pivotal role in numerous physiological functions, notably neuronal signaling and the contraction of cardiac muscles. The activation kinetics of ion channels usually commence with a stimulus triggering a coordinated conformational change in the channel protein. In the context of cardiac diseases, this process holds significant relevance. The resulting conformational change leads to the opening of a channel pore, selectively allowing ions to traverse the cell membrane. Notably, the molecular behavior of ion channels can be influenced by various agents, including neurotransmitters, hormones, and drugs.

Within the realm of cardiac diseases, understanding the cellular and molecular aspects of these fundamental processes becomes paramount. Cardiac diseases involve intricate research in the field of cardiac cellular electrophysiology. State-of-the-art molecular and biophysical techniques are applied to cardiac myocytes obtained from diverse experimental models to unravel the complexities of heart function. We encourage contributions employing innovative approaches to elucidate molecular mechanisms, thereby enhancing our understanding of the molecular basis of cardiac diseases from a multiscale perspective.

Dr. Jader Santos Cruz
Guest Editor

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Keywords

  • electrophysiology
  • cardiac diseases
  • electrical signals
  • electrical remodeling
  • channels dysfunction

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Published Papers (2 papers)

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Research

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18 pages, 3987 KiB  
Article
Cardioimmunology in Health and Diseases: Impairment of the Cardio-Spleno-Bone Marrow Axis Following Myocardial Infarction in Diabetes Mellitus
by Amankeldi A. Salybekov, Kanat Tashov, Yin Sheng, Ainur Salybekova, Yoshiko Shinozaki, Takayuki Asahara and Shuzo Kobayashi
Int. J. Mol. Sci. 2024, 25(21), 11833; https://doi.org/10.3390/ijms252111833 - 4 Nov 2024
Viewed by 1143
Abstract
A comprehensive understanding of the cardio-spleen-bone marrow immune cell axis is essential for elucidating the alterations occurring during the pathogenesis of diabetes mellitus (DM). This study investigates the dynamics of immune cell kinetics in DM after myocardial infarction (MI) over time. MI was [...] Read more.
A comprehensive understanding of the cardio-spleen-bone marrow immune cell axis is essential for elucidating the alterations occurring during the pathogenesis of diabetes mellitus (DM). This study investigates the dynamics of immune cell kinetics in DM after myocardial infarction (MI) over time. MI was induced in diabetic and healthy control groups using C57BL/N6 mice, with sacrifices occurring at days 1, 3, 7, and 28 post-MI to collect heart, peripheral blood (PB), spleen, and bone marrow (BM) samples. Cell suspensions from each organ were isolated and analyzed via flow cytometry. Additionally, the endothelial progenitor cell-colony-forming assay (EPC-CFA) was performed using mononuclear cells derived from BM, PB, and the spleen. The results indicated that, despite normal production in BM and the spleen, CD45+ cells were lower in the PB of DM mice at days 1 to 3. Further analysis revealed a reduction in total and pro-inflammatory neutrophils (N1s) in PB at days 1 to 3 and in the spleen at days 3 to 7 in DM mice, suggesting that DM-induced alterations in splenic neutrophils fail to meet the demand in PB and ischemic tissues. Infiltrating macrophages (total, M1, M2) were reduced at day 3 in the DM-ischemic heart, with total and M1 (days 1–3) and M2 (days 3–7) macrophages being significantly decreased in DM-PB compared to controls, indicating impaired macrophage recruitment and polarization in DM. Myeloid dendritic cells (mDCs) in the heart were higher from days 1 to 7, which corresponded with the enhanced recruitment of CD8+ cells from days 1 to 28 in the DM-infarcted myocardium. Total CD4+ cells decreased in DM-PB at days 1 to 3, suggesting a delayed adaptive immune response to MI. B cells were reduced in PB at days 1 to 3, in myocardium at day 3, and in the spleen at day 7, indicating compromised mobilization from BM. EPC-CFA results showed a marked decrease in definitive EPC colonies in the spleen and BM from days 1 to 28 in DM mice compared to controls in vitro, highlighting that DM severely impairs EPC colony-forming activity by limiting the differentiation of EPCs from primitive to definitive forms. Taking together, this study underscores significant disruptions in the cardio-spleen-bone marrow immune cell axis following MI in DM, revealing delayed innate and adaptive immune responses along with impaired EPC differentiation. Full article
(This article belongs to the Special Issue Cardiac Diseases: Molecular Mechanisms and Therapeutic Strategies)
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Review

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14 pages, 634 KiB  
Review
Viral Myocarditis as a Factor Leading to the Development of Heart Failure Symptoms, Including the Role of Parvovirus B19 Infection—Systematic Review
by Sebastian Krych, Agata Jęczmyk, Michał Jurkiewicz, Martyna Żurek, Małgorzata Jekiełek, Paweł Kowalczyk, Karol Kramkowski and Tomasz Hrapkowicz
Int. J. Mol. Sci. 2024, 25(15), 8127; https://doi.org/10.3390/ijms25158127 - 25 Jul 2024
Cited by 5 | Viewed by 2865
Abstract
Myocarditis (MC) is defined as an immunological inflammatory reaction with various etiologies, clinical presentations and prognoses within the myocardium. Currently, parvovirus B19 (PVB19) has become the main factor leading to this disease, replacing the previously dominant viruses A and B. In the case [...] Read more.
Myocarditis (MC) is defined as an immunological inflammatory reaction with various etiologies, clinical presentations and prognoses within the myocardium. Currently, parvovirus B19 (PVB19) has become the main factor leading to this disease, replacing the previously dominant viruses A and B. In the case of chronic heart failure with subsequent dilated cardiomyopathy, approximately 67% have a viral etiology, and most of them are the result of PVB19 infection. However, the analysis showed a correlation between PVB19 infection and the risk of developing inflammatory dilated cardiomyopathy (DCMi). PVB19 is detected in 23% of patients with DCMi. Chronic infection may also contribute to progressive left ventricular failure in patients with a history of MC. The above effect suggests the active replication of PVB19 only in heart biopsies with inflammation due to MC or DCMi. Moreover, the supply of IFN-β to suppress the active transcription of PVB19 accompanied by DCMi over a period of 6 months results in the normalization of NT-proBNP and an improvement in LVEF along with NYHA performance. The small number of reports on this topic and inaccuracies resulting from constantly conducted research and ongoing changes make it impossible to clearly answer the question of whether PVB19 is a factor inducing de novo MC and DCM or only accompanies the above conditions. However, large clinical cohort studies lead to the perception of PVB19 as a viral etiological agent capable of causing de novo MC together with DCMi. Full article
(This article belongs to the Special Issue Cardiac Diseases: Molecular Mechanisms and Therapeutic Strategies)
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