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Mitochondrial and Calcium Signaling in Human Health and Disease
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Mitochondrial and Calcium Signaling in Human Health and Disease

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

Deadline for manuscript submissions: closed (31 October 2022) | Viewed by 9160

Special Issue Editor

Prof. Dr. Krzysztof Zabłocki

E-Mail Website
Guest Editor
Laboratory of Cellular Metabolism, Nencki Institute of Experimental Biology PAS, 02-093 Warsaw, Poland
Interests: metabolism; mitochondria; bioenergetics; calcium signaling; vascular endothelium; muscle differentiation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Mitochondria are the central hub for cellular metabolism and provide energy to perform all cellular functions. Besides their critical role in bioenergetics, mitochondria are the site of cell death signalling events. Mitochondrial homeostasis is regulated by various metabolic inputs like nutrient availability and hormonal regulation, which also regulate Ca2+ dynamics. In response to various pathophysiological signals, mitochondria exhibit early alterations in their shape and function, which, may be explained by mitochondrial fission, fusion, structural remodelling, and mitochondrial permeability transition pore (MPTP) regulated swelling.

Calcium is thought to play an important role in regulating mitochondrial function. 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.

The Special Issue welcomes original research articles and reviews covering many aspects of molecular biology of mitochondrial and mitochondrial calcium.

Prof. Dr. Krzysztof Zabłocki
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 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.

Keywords

  • mitochondria
  • mitochondrial calcium
  • mitochondrial dynamics
  • MPTP

Published Papers (3 papers)

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Review

16 pages, 932 KiB  
Review
Mitochondrial Dysfunction and Therapeutic Perspectives in Cardiovascular Diseases
by Yu Liu, Yuejia Huang, Chong Xu, Peng An, Yongting Luo, Lei Jiao, Junjie Luo and Yongzhi Li
Int. J. Mol. Sci. 2022, 23(24), 16053; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232416053 - 16 Dec 2022
Cited by 16 | Viewed by 3323
Abstract
High mortality rates due to cardiovascular diseases (CVDs) have attracted worldwide attention. It has been reported that mitochondrial dysfunction is one of the most important mechanisms affecting the pathogenesis of CVDs. Mitochondrial DNA (mtDNA) mutations may result in impaired oxidative phosphorylation (OXPHOS), abnormal [...] Read more.
High mortality rates due to cardiovascular diseases (CVDs) have attracted worldwide attention. It has been reported that mitochondrial dysfunction is one of the most important mechanisms affecting the pathogenesis of CVDs. Mitochondrial DNA (mtDNA) mutations may result in impaired oxidative phosphorylation (OXPHOS), abnormal respiratory chains, and ATP production. In dysfunctional mitochondria, the electron transport chain (ETC) is uncoupled and the energy supply is reduced, while reactive oxygen species (ROS) production is increased. Here, we discussed and analyzed the relationship between mtDNA mutations, impaired mitophagy, decreased OXPHOS, elevated ROS, and CVDs from the perspective of mitochondrial dysfunction. Furthermore, we explored current potential therapeutic strategies for CVDs by eliminating mtDNA mutations (e.g., mtDNA editing and mitochondrial replacement), enhancing mitophagy, improving OXPHOS capacity (e.g., supplement with NAD+, nicotinamide riboside (NR), nicotinamide mononucleotide (NMN), and nano-drug delivery), and reducing ROS (e.g., supplement with Coenzyme Q10 and other antioxidants), and dissected their respective advantages and limitations. In fact, some therapeutic strategies are still a long way from achieving safe and effective clinical treatment. Although establishing effective and safe therapeutic strategies for CVDs remains challenging, starting from a mitochondrial perspective holds bright prospects. Full article
(This article belongs to the Special Issue Mitochondrial and Calcium Signaling in Human Health and Disease)
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19 pages, 2801 KiB  
Review
The Regulatory Roles of Mitochondrial Calcium and the Mitochondrial Calcium Uniporter in Tumor Cells
by Linlin Zhang, Jingyi Qi, Xu Zhang, Xiya Zhao, Peng An, Yongting Luo and Junjie Luo
Int. J. Mol. Sci. 2022, 23(12), 6667; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23126667 - 15 Jun 2022
Cited by 9 | Viewed by 2556
Abstract
Mitochondria, as the main site of cellular energy metabolism and the generation of oxygen free radicals, are the key switch for mitochondria-mediated endogenous apoptosis. Ca2+ is not only an important messenger for cell proliferation, but it is also an indispensable signal for [...] Read more.
Mitochondria, as the main site of cellular energy metabolism and the generation of oxygen free radicals, are the key switch for mitochondria-mediated endogenous apoptosis. Ca2+ is not only an important messenger for cell proliferation, but it is also an indispensable signal for cell death. Ca2+ participates in and plays a crucial role in the energy metabolism, physiology, and pathology of mitochondria. Mitochondria control the uptake and release of Ca2+ through channels/transporters, such as the mitochondrial calcium uniporter (MCU), and influence the concentration of Ca2+ in both mitochondria and cytoplasm, thereby regulating cellular Ca2+ homeostasis. Mitochondrial Ca2+ transport-related processes are involved in important biological processes of tumor cells including proliferation, metabolism, and apoptosis. In particular, MCU and its regulatory proteins represent a new era in the study of MCU-mediated mitochondrial Ca2+ homeostasis in tumors. Through an in-depth analysis of the close correlation between mitochondrial Ca2+ and energy metabolism, autophagy, and apoptosis of tumor cells, we can provide a valuable reference for further understanding of how mitochondrial Ca2+ regulation helps diagnosis and therapy. Full article
(This article belongs to the Special Issue Mitochondrial and Calcium Signaling in Human Health and Disease)
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18 pages, 1897 KiB  
Review
Mitochondria-Mediated Cardiovascular Benefits of Sodium-Glucose Co-Transporter 2 Inhibitors
by Siarhei A. Dabravolski, Alexander D. Zhuravlev, Andrey G. Kartuesov, Evgeny E. Borisov, Vasily N. Sukhorukov and Alexander N. Orekhov
Int. J. Mol. Sci. 2022, 23(10), 5371; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23105371 - 11 May 2022
Cited by 5 | Viewed by 2670
Abstract
Several recent cardiovascular trials of SGLT 2 (sodium-glucose cotransporter 2) inhibitors revealed that they could reduce adverse cardiovascular events in patients with T2DM (type 2 diabetes mellitus). However, the exact molecular mechanism underlying the beneficial effects that SGLT2 inhibitors have on the cardiovascular [...] Read more.
Several recent cardiovascular trials of SGLT 2 (sodium-glucose cotransporter 2) inhibitors revealed that they could reduce adverse cardiovascular events in patients with T2DM (type 2 diabetes mellitus). However, the exact molecular mechanism underlying the beneficial effects that SGLT2 inhibitors have on the cardiovascular system is still unknown. In this review, we focus on the molecular mechanisms of the mitochondria-mediated beneficial effects of SGLT2 inhibitors on the cardiovascular system. The application of SGLT2 inhibitors ameliorates mitochondrial dysfunction, dynamics, bioenergetics, and ion homeostasis and reduces the production of mitochondrial reactive oxygen species, which results in cardioprotective effects. Herein, we present a comprehensive overview of the impact of SGLT2 inhibitors on mitochondria and highlight the potential application of these medications to treat both T2DM and cardiovascular diseases. Full article
(This article belongs to the Special Issue Mitochondrial and Calcium Signaling in Human Health and Disease)
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