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Special Issue "Molecular Research on Cardiomyopathy"

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

Deadline for manuscript submissions: 30 April 2021.

Special Issue Editor

Dr. Cristi L. Galindo

Guest Editor
Western Kentucky University
Interests: fibrosis, Duchenne cardiomyopathy, BDNF, NRG, ErbB3

Special Issue Information

Dear Colleagues,

The field of cardiovascular medicine has broadened as technologies evolve. More importantly, clinically relevant discoveries have grown exponentially with genomics, improvements in stem cells, inter-organ and systemic approaches, and cardiotoxicity side-effects of cancer drugs and a variety of other therapeutics. It is becoming increasingly apparent that the heart is inexorably linked to multiple human disease conditions. As such, the molecular underpinnings of non-cardiac processes have emerged with new relevancy to cardiac disease. Contributions to this Special Issue will provide insights into novel mechanisms of action that contribute broadly to cardiomyopathies of multiple etiologies and suggest therapeutic interventions for meeting new challenges in heart health.

Dr. Cristi L. Galindo
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 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.

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

  • cardiomyopathy
  • genomics
  • gene expression
  • myocytes
  • fibrosis

Published Papers (2 papers)

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Research

Open AccessArticle
Reversal of the Inflammatory Responses in Fabry Patient iPSC-Derived Cardiovascular Endothelial Cells by CRISPR/Cas9-Corrected Mutation
Int. J. Mol. Sci. 2021, 22(5), 2381; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22052381 (registering DOI) - 27 Feb 2021
Abstract
The late-onset type of Fabry disease (FD) with GLA IVS4 + 919G > A mutation has been shown to lead to cardiovascular dysfunctions. In order to eliminate variations in other aspects of the genetic background, we established the isogenic control of induced pluripotent [...] Read more.
The late-onset type of Fabry disease (FD) with GLA IVS4 + 919G > A mutation has been shown to lead to cardiovascular dysfunctions. In order to eliminate variations in other aspects of the genetic background, we established the isogenic control of induced pluripotent stem cells (iPSCs) for the identification of the pathogenetic factors for FD phenotypes through CRISPR/Cas9 genomic editing. We adopted droplet digital PCR (ddPCR) to efficiently capture mutational events, thus enabling isolation of the corrected FD from FD-iPSCs. Both of these exhibited the characteristics of pluripotency and phenotypic plasticity, and they can be differentiated into endothelial cells (ECs). We demonstrated the phenotypic abnormalities in FD iPSC-derived ECs (FD-ECs), including intracellular Gb3 accumulation, autophagic flux impairment, and reactive oxygen species (ROS) production, and these abnormalities were rescued in isogenic control iPSC-derived ECs (corrected FD-ECs). Microarray profiling revealed that corrected FD-derived endothelial cells reversed the enrichment of genes in the pro-inflammatory pathway and validated the downregulation of NF-κB and the MAPK signaling pathway. Our findings highlighted the critical role of ECs in FD-associated vascular dysfunctions by establishing a reliable isogenic control and providing information on potential cellular targets to reduce the morbidity and mortality of FD patients with vascular complications. Full article
(This article belongs to the Special Issue Molecular Research on Cardiomyopathy)
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Open AccessArticle
Energy Metabolites as Biomarkers in Ischemic and Dilated Cardiomyopathy
Int. J. Mol. Sci. 2021, 22(4), 1999; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22041999 - 18 Feb 2021
Abstract
With more than 25 million people affected, heart failure (HF) is a global threat. As energy production pathways are known to play a pivotal role in HF, we sought here to identify key metabolic changes in ischemic- and non-ischemic HF by using a [...] Read more.
With more than 25 million people affected, heart failure (HF) is a global threat. As energy production pathways are known to play a pivotal role in HF, we sought here to identify key metabolic changes in ischemic- and non-ischemic HF by using a multi-OMICS approach. Serum metabolites and mRNAseq and epigenetic DNA methylation profiles were analyzed from blood and left ventricular heart biopsy specimens of the same individuals. In total we collected serum from n = 82 patients with Dilated Cardiomyopathy (DCM) and n = 51 controls in the screening stage. We identified several metabolites involved in glycolysis and citric acid cycle to be elevated up to 5.7-fold in DCM (p = 1.7 × 10−6). Interestingly, cardiac mRNA and epigenetic changes of genes encoding rate-limiting enzymes of these pathways could also be found and validated in our second stage of metabolite assessment in n = 52 DCM, n = 39 ischemic HF and n = 57 controls. In conclusion, we identified a new set of metabolomic biomarkers for HF. We were able to identify underlying biological cascades that potentially represent suitable intervention targets. Full article
(This article belongs to the Special Issue Molecular Research on Cardiomyopathy)
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