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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 January 2022) | Viewed by 8482

Special Issue Editors

Dr. Tarik Smani

E-Mail Website
Guest Editor
Department of Medical Physiology and Biophysics, Faculty of Medicine, University of Seville, 41009 Seville, Spain
Interests: calcium signaling; STIM1; Orai1; TRPC channel; angiogenesis
Special Issues, Collections and Topics 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 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. 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 (3 papers)

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Research

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16 pages, 3511 KiB  
Article
miR-16-5p Suppression Protects Human Cardiomyocytes against Endoplasmic Reticulum and Oxidative Stress-Induced Injury
by Rocío Toro, Alexandra Pérez-Serra, Alipio Mangas, Oscar Campuzano, Georgia Sarquella-Brugada, Maribel Quezada-Feijoo, Mónica Ramos, Martin Alcalá, Esther Carrera, Carlos García-Padilla, Diego Franco and Fernando Bonet
Int. J. Mol. Sci. 2022, 23(3), 1036; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23031036 - 18 Jan 2022
Cited by 17 | Viewed by 2416
Abstract
Oxidative stress, defined as the excess production of reactive oxygen species (ROS) relative to antioxidant defense, plays a significant role in the development of cardiovascular diseases. Endoplasmic reticulum (ER) stress has emerged as an important source of ROS and its modulation could be [...] Read more.
Oxidative stress, defined as the excess production of reactive oxygen species (ROS) relative to antioxidant defense, plays a significant role in the development of cardiovascular diseases. Endoplasmic reticulum (ER) stress has emerged as an important source of ROS and its modulation could be cardioprotective. Previously, we demonstrated that miR-16-5p is enriched in the plasma of ischemic dilated cardiomyopathy (ICM) patients and promotes ER stress-induced apoptosis in cardiomyocytes in vitro. Here, we hypothesize that miR-16-5p might contribute to oxidative stress through ER stress induction and that targeting miR-16-5p may exert a cardioprotective role in ER stress-mediated cardiac injury. Analysis of oxidative markers in the plasma of ICM patients demonstrates that oxidative stress is associated with ICM. Moreover, we confirm that miR-16-5p overexpression promotes oxidative stress in AC16 cardiomyoblasts. We also find that, in response to tunicamycin-induced ER stress, miR-16-5p suppression decreases apoptosis, inflammation and cardiac damage via activating the ATF6-mediated cytoprotective pathway. Finally, ATF6 is identified as a direct target gene of miR-16-5p by dual-luciferase reporter assays. Our results indicate that miR-16-5p promotes ER stress and oxidative stress in cardiac cells through regulating ATF6, suggesting that the inhibition of miR-16-5p has potential as a therapeutic approach to protect the heart against ER and oxidative stress-induced injury. Full article
(This article belongs to the Special Issue Calcium Mishandling, Inflammation, microRNAs and Their Role in the Adverse Cardiovascular Remodelling)
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17 pages, 3399 KiB  
Article
Genetic Deletion of NOD1 Prevents Cardiac Ca2+ Mishandling Induced by Experimental Chronic Kidney Disease
by Marta Gil-Fernández, José Alberto Navarro-García, Almudena Val-Blasco, Laura González-Lafuente, José Carlos Martínez, Angélica Rueda, Maria Tamayo, José Luis Morgado, Carlos Zaragoza, Luis Miguel Ruilope, Carmen Delgado, Gema Ruiz-Hurtado and María Fernández-Velasco
Int. J. Mol. Sci. 2020, 21(22), 8868; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21228868 - 23 Nov 2020
Cited by 5 | Viewed by 2651
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
(This article belongs to the Special Issue Calcium Mishandling, Inflammation, microRNAs and Their Role in the Adverse Cardiovascular Remodelling)
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Review

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12 pages, 854 KiB  
Review
Urocortin Role in Ischemia Cardioprotection and the Adverse Cardiac Remodeling
by Eva M. Calderón-Sánchez, Débora Falcón, Marta Martín-Bórnez, Antonio Ordoñez and Tarik Smani
Int. J. Mol. Sci. 2021, 22(22), 12115; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222212115 - 09 Nov 2021
Cited by 2 | Viewed by 2490
Abstract
Despite the considerable progress in strategies of myocardial protection, ischemic heart diseases (IHD) and consequent heart failure (HF) remain the main cause of mortality worldwide. Several procedures are used routinely to guarantee the prompt and successful reestablishment of blood flow to preserve the [...] Read more.
Despite the considerable progress in strategies of myocardial protection, ischemic heart diseases (IHD) and consequent heart failure (HF) remain the main cause of mortality worldwide. Several procedures are used routinely to guarantee the prompt and successful reestablishment of blood flow to preserve the myocardial viability of infarcted hearts from ischemia injuries. However, ischemic heart reperfusion/revascularization triggers additional damages that occur when oxygen-rich blood re-enters the vulnerable myocardial tissue, which is a phenomenon known as ischemia and reperfusion (I/R) syndrome. Complications of I/R injuries provoke the adverse cardiac remodeling, involving inflammation, mishandling of Ca2+ homeostasis, apoptotic genes activation, cardiac myocytes loss, etc., which often progress toward HF. Therefore, there is an urgent need to develop new cardioprotective therapies for IHD and HF. Compelling evidence from animal studies and pilot clinical trials in HF patients suggest that urocortin (Ucn) isoforms, which are peptides associated with stress and belonging to the corticotropin releasing factor family, have promising potential to improve cardiovascular functions by targeting many signaling pathways at different molecular levels. This review highlights the current knowledge on the role of urocortin isoforms in cardioprotection, focusing on its acute and long-term effects. Full article
(This article belongs to the Special Issue Calcium Mishandling, Inflammation, microRNAs and Their Role in the Adverse Cardiovascular Remodelling)
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