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Special Issue "Calcium Mishandling, Inflammation, microRNAs and Their Role in the Adverse Cardiovascular Remodelling"

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 (10 September 2021).

Special Issue Editors

Dr. Tarik Smani
E-Mail Website
Guest Editor
Department of Medical Physiology and Biophysics, Institute of Biomedicine of Seville (IBiS), University of Seville, Seville, Spain
Interests: calcium signaling; STIM1; Orai1; TRPC channel; angiogenesis
Special Issues and Collections in MDPI journals
Dr. Raquel Del Toro
E-Mail Website
Guest Editor
Department of Medical Physiology and Biophysics, Institute of Biomedicine of Seville, University of Seville, Sevilla, Spain
Interests: inflammation; microRNAs; Cardiac and vascular remodelling; cardiac protection

Special Issue Information

Dear Colleagues,

The prevalence of heart failure (HF) consequent to adverse cardiac remodeling continues to rise, increasing the rate of morbidity and mortality worldwide. Cardiovascular adverse remodeling is a complex process involving calcium (Ca2+) mishandling, inflammation, and cardiac myocyte death, among other mechanisms. Although substantial progress has been made and a significant amount of data has accumulated in recent years, many aspects of inflammation, the dysregulation of the intracellular Ca2+ concentration ([Ca2+]i), and the role of miRNAs in post-transcriptional gene regulation remain unexplored. The objective of this Special Issue is to highlight the impact of inflammation and [Ca2+]i mishandling on adverse cardiac remodeling. In addition, this Special Issue will also discuss the role of miRNAs in the post-transcriptional regulation of genes associated with [Ca2+]i and/or inflammation, which can influence cardiac remodeling and HF progression. We welcome original research and up-to-date review articles on any of these aspects.

Dr. Tarik Smani
Dr. Raquel Del Toro
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.

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.

Published Papers (1 paper)

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Research

Article
Genetic Deletion of NOD1 Prevents Cardiac Ca2+ Mishandling Induced by Experimental Chronic Kidney Disease
Int. J. Mol. Sci. 2020, 21(22), 8868; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21228868 - 23 Nov 2020
Viewed by 933
Abstract
Risk of cardiovascular disease (CVD) increases considerably as renal function declines in chronic kidney disease (CKD). Nucleotide-binding oligomerization domain-containing protein 1 (NOD1) has emerged as a novel innate immune receptor involved in both CVD and CKD. Following activation, NOD1 undergoes a conformational change [...] Read more.
Risk of cardiovascular disease (CVD) increases considerably as renal function declines in chronic kidney disease (CKD). Nucleotide-binding oligomerization domain-containing protein 1 (NOD1) has emerged as a novel innate immune receptor involved in both CVD and CKD. Following activation, NOD1 undergoes a conformational change that allows the activation of the receptor-interacting serine/threonine protein kinase 2 (RIP2), promoting an inflammatory response. We evaluated whether the genetic deficiency of Nod1 or Rip2 in mice could prevent cardiac Ca2+ mishandling induced by sixth nephrectomy (Nx), a model of CKD. We examined intracellular Ca2+ dynamics in cardiomyocytes from Wild-type (Wt), Nod1−/− and Rip2−/− sham-operated or nephrectomized mice. Compared with Wt cardiomyocytes, Wt-Nx cells showed an impairment in the properties and kinetics of the intracellular Ca2+ transients, a reduction in both cell shortening and sarcoplasmic reticulum Ca2+ load, together with an increase in diastolic Ca2+ leak. Cardiomyocytes from Nod1−/−-Nx and Rip2−/−-Nx mice showed a significant amelioration in Ca2+ mishandling without modifying the kidney impairment induced by Nx. In conclusion, Nod1 and Rip2 deficiency prevents the intracellular Ca2+ mishandling induced by experimental CKD, unveiling new innate immune targets for the development of innovative therapeutic strategies to reduce cardiac complications in patients with CKD. Full article
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