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: 31 May 2025 | Viewed by 1689

Special Issue Editors


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Guest Editor
Department of Biochemistry, Molecular Biology and Physiology, IBGM—Universidad de Valladolid, Valladolid, Spain
Interests: mitochondria; Ca2+; aging; heart; organelle contactology; bioenergetics

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

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Keywords

  • mitochondria
  • calcium
  • MCU
  • uniporter
  • NCLX
  • energy metabolism
  • disease
  • MAMs
  • signaling

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Published Papers (1 paper)

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Research

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 1355
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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