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Cells
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Cellular Mechanisms in Mitochondrial Function and Calcium Signaling
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Cellular Mechanisms in Mitochondrial Function and Calcium Signaling

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Metabolism".

Deadline for manuscript submissions: 30 November 2025 | Viewed by 2607

Special Issue Editors

Dr. Sergio De la Fuente

E-Mail Website
Guest Editor
Department of Biochemistry, Molecular Biology and Physiology, IBGM—Universidad de Valladolid, Valladolid, Spain
Interests: mitochondria; Ca2+; aging; heart; organelle contactology; bioenergetics
Dr. Jaime Santo-Domingo

E-Mail Website
Guest Editor
Department of Biochemistry, Molecular Biology, and Physiology, IBGM—Universidad de Valladolid, Valladolid, Spain
Interests: mitochondria; calcium; energy metabolism; aging; beta cell

Special Issue Information

Dear Colleagues,

Calcium (Ca2+) is a ubiquitous second messenger whose signaling is regulated by compartmentalization and transport across several cellular membranes. Ca2+ controls a wide range of cellular processes, from cellular contraction to exocytosis or gene expression. Mitochondria transform the free energy stored in highly reduced compounds into chemical energy in the form of ATP to support energy-consuming cellular processes across the cell. Beyond this well-known role, mitochondria are crucial in apoptosis, metabolite biosynthesis, and cellular immune response, among other cellular processes. Mitochondrial function is highly integrated within the specific cellular context of each cell, and Ca2+ signals play a key role in maintaining it. The functional interaction between cellular Ca2+ signaling and mitochondria is complex; mitochondria can contribute to trigger and shape cytosolic Ca2+ signals while also sensing, decoding, and responding to such Ca2+ signals. Moreover, they frequently also involve other organelles such as the plasma membrane or the endoplasmic/sarcoplasmic reticulum. This Special Issue aims to publish manuscripts that explore the intricate relationships between mitochondria and cellular calcium homeostasis in both health and disease.

Dr. Sergio De la Fuente
Dr. Jaime Santo-Domingo
Guest Editors

Manuscript Submission Information

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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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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
  • calcium
  • MCU
  • uniporter
  • NCLX
  • energy metabolism
  • disease
  • MAMs
  • signaling

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Published Papers (2 papers)

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Research

24 pages, 5385 KiB  
Article
Highly Oligomeric DRP1 Strategic Positioning at Mitochondria–Sarcoplasmic Reticulum Contacts in Adult Murine Heart Through ACTIN Anchoring
by Celia Fernandez-Sanz, Sergio De la Fuente, Zuzana Nichtova, Marilen Federico, Stephane Duvezin-Caubet, Sebastian Lanvermann, Hui-Ying Tsai, Yanguo Xin, Gyorgy Csordas, Wang Wang, Arnaud Mourier and Shey-Shing Sheu
Cells 2025, 14(16), 1259; https://doi.org/10.3390/cells14161259 - 14 Aug 2025
Viewed by 456
Abstract
Mitochondrial fission and fusion appear to be relatively infrequent in cardiac cells compared to other cell types; however, the proteins involved in these events are highly expressed in adult cardiomyocytes (ACM). Therefore, these proteins likely have additional non-canonical roles. We have previously shown [...] Read more.
Mitochondrial fission and fusion appear to be relatively infrequent in cardiac cells compared to other cell types; however, the proteins involved in these events are highly expressed in adult cardiomyocytes (ACM). Therefore, these proteins likely have additional non-canonical roles. We have previously shown that DRP1 not only participates in mitochondrial fission processes but also regulates mitochondrial bioenergetics in cardiac tissue. However, it is still unknown where the DRP1 that does not participate in mitochondrial fission is located and what its role is at those non-fission spots. Therefore, this manuscript will clarify whether oligomeric DRP1 is located at the SR–mitochondria interface, a specific region that harbors the Ca2+ microdomains created by Ca2+ release from the SR through the RyR2. The high Ca2+ microdomains and the subsequent Ca2+ uptake by mitochondria through the mitochondrial Ca2+ uniporter complex (MCUC) are essential to regulate mitochondrial bioenergetics during excitation–contraction (EC) coupling. Herein, we aimed to test the hypothesis that mitochondria-bound DRP1 preferentially accumulates at the mitochondria–SR contacts to deploy its function on regulating mitochondrial bioenergetics and that this strategic position is modulated by calcium in a beat-to-beat manner. In addition, the mechanism responsible for such a biased distribution and its functional implications was investigated. High-resolution imaging approaches, cell fractionation, Western blot, 2D blue native gel electrophoresis, and immunoprecipitations were applied to both electrically paced ACM and Langendorff-perfused beating hearts to elucidate the mechanisms of the strategic DRP1 localization. Our data show that in ACM, mitochondria-bound DRP1 clusters in high molecular weight protein complexes at mitochondria-associated membrane (MAM). This clustering requires DRP1 interaction with β-ACTIN and is fortified by EC coupling-mediated Ca2+ transients. In ACM, DRP1 is anchored at the mitochondria–SR contacts through interactions with β-ACTIN and Ca2+ transients, playing a fundamental role in regulating mitochondrial physiology. Full article
(This article belongs to the Special Issue Cellular Mechanisms in Mitochondrial Function and Calcium Signaling)
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12 pages, 2022 KiB  
Article
Subcellular Compartmentalization of Glucose Mediated Insulin Secretion
by Zhongying Wang, Tatyana Gurlo, Leslie S. Satin, Scott E. Fraser and Peter C. Butler
Cells 2025, 14(3), 198; https://doi.org/10.3390/cells14030198 - 29 Jan 2025
Viewed by 1721
Abstract
Regulation of blood glucose levels depends on the property of beta cells to couple glucose sensing with insulin secretion. This is accomplished by the concentration-dependent flux of glucose through glycolysis and oxidative phosphorylation, generating ATP. The resulting rise in cytosolic ATP/ADP inhibits K [...] Read more.
Regulation of blood glucose levels depends on the property of beta cells to couple glucose sensing with insulin secretion. This is accomplished by the concentration-dependent flux of glucose through glycolysis and oxidative phosphorylation, generating ATP. The resulting rise in cytosolic ATP/ADP inhibits KATP channels, inducing membrane depolarization and Ca2+ influx, which prompts insulin secretion. Evidence suggests that this coupling of glucose sensing with insulin secretion may be compartmentalized in the submembrane regions of the beta cell. We investigated the subcellular responses of key components involved in this coupling and found mitochondria in the submembrane zone, some tethered to the cytoskeleton near capillaries. Using Fluorescent Lifetime Imaging Microscopy (FLIM), we observed that submembrane mitochondria were the fastest to respond to glucose. In the most glucose-responsive beta cells, glucose triggers rapid, localized submembrane increases in ATP and Ca2+ as synchronized ~4-min oscillations, consistent with pulsatile insulin release after meals. These findings are consistent with the hypothesis that glucose sensing is coupled with insulin secretion in the submembrane zone of beta cells. This zonal adaptation would enhance both the speed and energy efficiency of beta cell responses to glucose, as only a subset of the most accessible mitochondria would be required to trigger insulin secretion. Full article
(This article belongs to the Special Issue Cellular Mechanisms in Mitochondrial Function and Calcium Signaling)
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