Molecular Mechanisms of Cardiac Development and 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: closed (31 March 2024) | Viewed by 60797
Special Issue Editors
Interests: vessel formation in development and disease; transcriptional control; epigenetics; cardiovascular disease
Special Issues, Collections and Topics in MDPI journals
Interests: vessel formation in development and disease; transcriptional control; epigenetics; cardiovascular disease
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
The heart is the first organ that forms and functions during embryonic development; and it must continue to work without interruption throughout one’s lifetime. In early embryonic development, the cardiac crescent contains progenitor cells of the first and second heart fields, which will mainly develop into the left ventricle/proportion of the atria and the right ventricle/outflow tract/atria, respectively. The contribution of epicardial, endocardial, sinus venosus, and hematopoietic-derived cells to the heart is still controversial. Although several important regulators of cardiac development have been identified, with this Special Issue, we aim to contribute to the knowledge of the molecular mechanisms of cardiac development and disease. Many previous studies have focused on cardiomyocyte development, but relatively little is known of how different cardiomyocyte subpopulations and other cells types, i.e., fibroblasts, endothelial, smooth muscle, epicardial, endocardial, and immune cells, contribute to heart morphology and function.
In contrast to lower vertebrates, cardiac development is finished in mammals soon after birth, and regeneration capacity becomes extremely limited. Nevertheless, cardiomyocyte proliferation is a prerequisite for cardiac regeneration in adults. Several transgenic mouse models have been reported to have an increased cardiomyocyte proliferation and improved recovery after cardiac injury. However, translation to clinical practice is limited due to ethical reasons and the risk of tumor development. In zebrafish, lineage tracing studies after injury showed that newly formed cardiac cells are derived from pre-existing, de-differentiating cardiomyocytes instead of a pool of cardiac progenitors. In neonatal mice, a subset of cardiomyocytes seems to be in a permissive (embryonic) state, which allows for re-entry in the cell cycle and repair after injury. Thus, identifying the molecular signature of this subset of cells would be of interest to direct cardiac repair in the future.
In addition to the evident problem in stimulating cardiomyocyte proliferation for repair after injury, several additional points must be considered. Increased cardiomyocyte repair needs an additional adequate blood supply (angiogenesis) for proper cardiac function. Damaged cells must be removed by immune cells and the tissue temporarily stabilized by a fibrotic response. However, excessive or prolonged immune and fibroblast activation will result in additional damage and impaired function due to increased tissue stiffness. Thus, for efficient cardiac repair after injury, cardiomyocyte proliferation and the adequate timing of angiogenesis, immune, and fibrotic response must be well-orchestrated.
This Special Issue of the International Journal of Molecular Sciences will bring together the most recent advances in understanding of the various aspects of the molecular regulation of cardiac development and disease, from basic science to applied therapeutic approaches, and will provide new insights into the complex regulation of cardiac development, disease, regeneration, and the different cell types involved.
Prof. Dr. Kay-Dietrich Wagner
Dr. Nicole Wagner
Guest Editors
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Keywords
cardiac development
cardiac repair
regeneration
cardiac cell-cell interaction
fibrosis
remodeling
molecular mechanisms
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