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Special Issue "Cardiac Repair and Regeneration: New Molecular Mechanisms and Therapeutics 2.0"

Special Issue Editors

Dr. Mohsin Khan
E-Mail Website
Guest Editor
Department of Physiology, Center for Metabolic Disease Research, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA
Interests: stem cells; cardiac repair; myocardial infarction; MicroRNAs
Special Issues, Collections and Topics in MDPI journals
Dr. Ronald Vagnozzi
E-Mail Website
Guest Editor
1. Department of Pediatrics, University of Cincinnati, Cincinnati, OH 45267, USA
2. Division of Molecular Cardiovascular Biology and The Heart Institute, Cincinnati Children's Hospital, Cincinnati, OH 45229, USA
Interests: cardiology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The adult heart is largely a postmitotic organ with limited cellular turnover during one’s lifetime. In the face of injury, adult cardiomyocytes undergo adverse remodeling and death, severely compromising cardiac structure and function. Over the years, several strategies have evolved with the goal to promote cardiac repair and regeneration in response to myocardial damage. This Special Issue explores the new molecular mechanisms and state-of-the-art therapeutics, including the strategies targeting cardiomyocyte cell cycle activation and proliferation, stem-cell-mediated cardiac repair, role of immune cells in cardiac repair, and extracellular vesicles in cardiac repair and regeneration. 

Dr. Mohsin Khan
Dr. Tamer Mohamed
Dr. Ronald Vagnozzi
Guest Editors

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 papers will be 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.

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Keywords

  • cardiac repair
  • regeneration
  • myocardial injury
  • cardiomyocyte cell cycle
  • proliferation
  • stem cells
  • paracrine factors
  • extracellular vesicles
  • immune cells
  • exosomes

Related Special Issue

Published Papers (2 papers)

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Research

Article
Dexmedetomidine Promotes Lipopolysaccharide-Induced Differentiation of Cardiac Fibroblasts and Collagen I/III Synthesis through α2A Adrenoreceptor-Mediated Activation of the PKC-p38-Smad2/3 Signaling Pathway in Mice
Int. J. Mol. Sci. 2021, 22(23), 12749; https://doi.org/10.3390/ijms222312749 - 25 Nov 2021
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Abstract
Dexmedetomidine (DEX), a selective α2 adrenergic receptor (AR) agonist, is commonly used as a sedative drug during critical illness. In the present study, we explored a novel accelerative effect of DEX on cardiac fibroblast (CF) differentiation mediated by LPS and clarified its [...] Read more.
Dexmedetomidine (DEX), a selective α2 adrenergic receptor (AR) agonist, is commonly used as a sedative drug during critical illness. In the present study, we explored a novel accelerative effect of DEX on cardiac fibroblast (CF) differentiation mediated by LPS and clarified its potential mechanism. LPS apparently increased the expression of α-SMA and collagen I/III and the phosphorylation of p38 and Smad-3 in the CFs of mice. These effects were significantly enhanced by DEX through increasing α2A-AR expression in CFs after LPS stimulation. The CFs from α2A-AR knockout mice were markedly less sensitive to DEX treatment than those of wild-type mice. Inhibition of protein kinase C (PKC) abolished the enhanced effects of DEX on LPS-induced differentiation of CFs. We also found that the α-SMA level in the second-passage CFs was much higher than that in the nonpassage and first-passage CFs. However, after LPS stimulation, the TNF-α released from the nonpassage CFs was much higher than that in the first- and second-passage CFs. DEX had no effect on LPS-induced release of TNF-α and IL-6 from CFs. Further investigation indicated that DEX promoted cardiac fibrosis and collagen I/III synthesis in mice exposed to LPS for four weeks. Our results demonstrated that DEX effectively accelerated LPS-induced differentiation of CFs to myofibroblasts through the PKC-p38-Smad2/3 signaling pathway by activating α2A-AR. Full article
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Article
PRC1 Stabilizes Cardiac Contraction by Regulating Cardiac Sarcomere Assembly and Cardiac Conduction System Construction
Int. J. Mol. Sci. 2021, 22(21), 11368; https://doi.org/10.3390/ijms222111368 - 21 Oct 2021
Viewed by 274
Abstract
Cardiac development is a complex process that is strictly controlled by various factors, including PcG protein complexes. Several studies have reported the critical role of PRC2 in cardiogenesis. However, little is known about the regulation mechanism of PRC1 in embryonic heart development. To [...] Read more.
Cardiac development is a complex process that is strictly controlled by various factors, including PcG protein complexes. Several studies have reported the critical role of PRC2 in cardiogenesis. However, little is known about the regulation mechanism of PRC1 in embryonic heart development. To gain more insight into the mechanistic role of PRC1 in cardiogenesis, we generated a PRC1 loss-of-function zebrafish line by using the CRISPR/Cas9 system targeting rnf2, a gene encoding the core subunit shared by all PRC1 subfamilies. Our results revealed that Rnf2 is not involved in cardiomyocyte differentiation and heart tube formation, but that it is crucial to maintaining regular cardiac contraction. Further analysis suggested that Rnf2 loss-of-function disrupted cardiac sarcomere assembly through the ectopic activation of non-cardiac sarcomere genes in the developing heart. Meanwhile, Rnf2 deficiency disrupts the construction of the atrioventricular canal and the sinoatrial node by modulating the expression of bmp4 and other atrioventricular canal marker genes, leading to an impaired cardiac conduction system. The disorganized cardiac sarcomere and defective cardiac conduction system together contribute to defective cardiac contraction. Our results emphasize the critical role of PRC1 in the cardiac development. Full article
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