Current Strategies for Cell-Based Cardiac Therapies

A special issue of Journal of Cardiovascular Development and Disease (ISSN 2308-3425). This special issue belongs to the section "Cardiac Development and Regeneration".

Deadline for manuscript submissions: closed (31 October 2023) | Viewed by 2211

Special Issue Editors


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Guest Editor
Amsterdam Cardiovascular Sciences, Department of Physiology, Amsterdam University Medical Centers, De Boelelaan 1108, 1081 HZ Amsterdam, The Netherlands
Interests: wnt signaling; sarcomere development; cardiomyocyte proliferation; hiPSC-CMs

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Guest Editor
1. Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA
2. Department of Pediatrics, Stanford University, Stanford, CA 94305, USA
Interests: cardiac conduction system development and disease

Special Issue Information

Dear Colleagues,

Cardiac injury, including blunt cardiac injury and penetrating cardiac injury, can result in a variety of specific injuries to the heart, the most common of which is myocardial contusion, a bruise (contusion) to the heart after an injury. Other potential injuries include septal defects and valvular failures, and the right ventricle is thought to be most commonly affected.

Autologous tissue therapy means that are removed from, and applied to, the same person, i.e., the donor and the recipient, are the same. The holy grail in translational cardiology is the repair of cardiac injury with autologous tissue or locally regenerate damaged myocardium or conduction systems. Autologous cell-based cardiac therapies have emerged as among the most promising strategies for treating heart injury. Furthermore, these new strategies could be closer to reality than ever with the advent of patient-specific pluripotent stem cell sources for cell and gene (editing) therapies. This Special Issue will be dedicated to novel technologies in mammalian cardiac cell-subtype generation and integration and explore strategies for local regeneration of the heart myocardium or conduction system.

Dr. Jan W. Buikema
Dr. William Rowland Goodyer
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 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. Journal of Cardiovascular Development and Disease is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • hiPSC-CM
  • cardiomyocyte cell therapy
  • cardiac repair
  • cardiac regeneration
  • hiPSC
  • conduction system
  • myocardium

Published Papers (1 paper)

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Review

21 pages, 587 KiB  
Review
Pharmaceutical Therapies for Necroptosis in Myocardial Ischemia–Reperfusion Injury
by Yinchang Zhang, Yantao Zhang, Jinlong Zang, Yongnan Li and Xiangyang Wu
J. Cardiovasc. Dev. Dis. 2023, 10(7), 303; https://doi.org/10.3390/jcdd10070303 - 17 Jul 2023
Cited by 4 | Viewed by 2018
Abstract
Cardiovascular disease morbidity/mortality are increasing due to an aging population and the rising prevalence of diabetes and obesity. Therefore, innovative cardioprotective measures are required to reduce cardiovascular disease morbidity/mortality. The role of necroptosis in myocardial ischemia–reperfusion injury (MI–RI) is beyond doubt, but the [...] Read more.
Cardiovascular disease morbidity/mortality are increasing due to an aging population and the rising prevalence of diabetes and obesity. Therefore, innovative cardioprotective measures are required to reduce cardiovascular disease morbidity/mortality. The role of necroptosis in myocardial ischemia–reperfusion injury (MI–RI) is beyond doubt, but the molecular mechanisms of necroptosis remain incompletely elucidated. Growing evidence suggests that MI–RI frequently results from the superposition of multiple pathways, with autophagy, ferroptosis, and CypD-mediated mitochondrial damage, and necroptosis all contributing to MI–RI. Receptor-interacting protein kinases (RIPK1 and RIPK3) as well as mixed lineage kinase domain-like pseudokinase (MLKL) activation is accompanied by the activation of other signaling pathways, such as Ca2+/calmodulin-dependent protein kinase II (CaMKII), NF-κB, and JNK-Bnip3. These pathways participate in the pathological process of MI–RI. Recent studies have shown that inhibitors of necroptosis can reduce myocardial inflammation, infarct size, and restore cardiac function. In this review, we will summarize the molecular mechanisms of necroptosis, the links between necroptosis and other pathways, and current breakthroughs in pharmaceutical therapies for necroptosis. Full article
(This article belongs to the Special Issue Current Strategies for Cell-Based Cardiac Therapies)
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