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Special Issue "Mitochondrial Calcium Signaling"

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

Deadline for manuscript submissions: 31 October 2020.

Special Issue Editors

Dr. Anna Raffaello
Website
Guest Editor
Department of Biomedical Sciences, University of Padova, Padova, Italy
Interests: mitochondria; calcium; mitochondrial calcium uniporter; skeletal muscle physiology
Dr. Denis Vecellio Reane

Guest Editor
Department of Biomedical Sciences, University of Padova, Padova, Italy
Interests: mitochondria; calcium; mitochondrial calcium uniporter; skeletal muscle physiology

Special Issue Information

Dear Colleagues,

Mitochondrial calcium has long been recognized as a fundamental signal in a plethora of cellular functions, ranging from the control of metabolism and ATP production to the regulation of cell death.

In the last ten years, we have witnessed an explosion of basic and translational research studies aiming to clarify the role of this crucial signal molecule. This was possible thanks to the identification of the long-sought molecular identity of the mitochondrial calcium uniporter complex that allowed the development of several tools to alter mitochondrial calcium.

The aim of this Special Issue is to bring together reviews and original papers on the composition and regulation of the complex and on the physiopathological function of mitochondrial calcium uptake.

We believe that there would be great interest in such a topic due to the regulation and stoichiometry of the components of the channel, the regulation of its activity, and the role in tissue homeostasis.

Dr. Anna Raffaello
Dr. Denis Vecellio Reane
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.

Keywords

  • mitochondrial calcium uniporter
  • calcium signaling
  • EF-hand proteins
  • mitochondria
  • signal transduction
  • ion channels
  • calcium dysregulation
  • calcium probes

Published Papers (2 papers)

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Review

Open AccessReview
The Physiological and Pathological Roles of Mitochondrial Calcium Uptake in Heart
Int. J. Mol. Sci. 2020, 21(20), 7689; https://doi.org/10.3390/ijms21207689 - 17 Oct 2020
Abstract
Calcium ion (Ca2+) plays a critical role in the cardiac mitochondria function. Ca2+ entering the mitochondria is necessary for ATP production and the contractile activity of cardiomyocytes. However, excessive Ca2+ in the mitochondria results in mitochondrial dysfunction and cell [...] Read more.
Calcium ion (Ca2+) plays a critical role in the cardiac mitochondria function. Ca2+ entering the mitochondria is necessary for ATP production and the contractile activity of cardiomyocytes. However, excessive Ca2+ in the mitochondria results in mitochondrial dysfunction and cell death. Mitochondria maintain Ca2+ homeostasis in normal cardiomyocytes through a comprehensive regulatory mechanism by controlling the uptake and release of Ca2+ in response to the cellular demand. Understanding the mechanism of modulating mitochondrial Ca2+ homeostasis in the cardiomyocyte could bring new insights into the pathogenesis of cardiac disease and help developing the strategy to prevent the heart from damage at an early stage. In this review, we summarized the latest findings in the studies on the cardiac mitochondrial Ca2+ homeostasis, focusing on the regulation of mitochondrial calcium uptake, which acts as a double-edged sword in the cardiac function. Specifically, we discussed the dual roles of mitochondrial Ca2+ in mitochondrial activity and the impact on cardiac function, the molecular basis and regulatory mechanisms, and the potential future research interest. Full article
(This article belongs to the Special Issue Mitochondrial Calcium Signaling)
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Open AccessReview
Diabetes Mellitus, Mitochondrial Dysfunction and Ca2+-Dependent Permeability Transition Pore
Int. J. Mol. Sci. 2020, 21(18), 6559; https://doi.org/10.3390/ijms21186559 - 08 Sep 2020
Cited by 1
Abstract
Diabetes mellitus is one of the most common metabolic diseases in the developed world, and is associated either with the impaired secretion of insulin or with the resistance of cells to the actions of this hormone (type I and type II diabetes, respectively). [...] Read more.
Diabetes mellitus is one of the most common metabolic diseases in the developed world, and is associated either with the impaired secretion of insulin or with the resistance of cells to the actions of this hormone (type I and type II diabetes, respectively). In both cases, a common pathological change is an increase in blood glucose—hyperglycemia, which eventually can lead to serious damage to the organs and tissues of the organism. Mitochondria are one of the main targets of diabetes at the intracellular level. This review is dedicated to the analysis of recent data regarding the role of mitochondrial dysfunction in the development of diabetes mellitus. Specific areas of focus include the involvement of mitochondrial calcium transport systems and a pathophysiological phenomenon called the permeability transition pore in the pathogenesis of diabetes mellitus. The important contribution of these systems and their potential relevance as therapeutic targets in the pathology are discussed. Full article
(This article belongs to the Special Issue Mitochondrial Calcium Signaling)
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Potential Topics:

  • Mitochondrial Calcium Signaling in pancreatic beta cells
  • Regulation of mitochondrial calcium homeostasis by the Bcl-2 family of proteins
  • A review devoted to alterations in calcium transport systems in the mitochondria of different tissues in diabetes mellitus
  • Different sensitivity to ruthenium-based inhibitors of the mitochondrial calcium uniporter complex of control and MICU1- and MICU2-ablated Trypanosoma cruzi
  • ER-mitochondria contact sites and how to detect them
  • The effect of deflazacort treatment on the functioning of skeletal muscle mitochondria in Duchenne muscular dystrophy (DMD)
  • Mitochondrial Ca2+ signalling in MCU knockout C. elegans worms
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