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Mitochondrial Function in Human Health and Disease: 3rd Edition

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

Deadline for manuscript submissions: 25 June 2026 | Viewed by 281

Special Issue Editor

Department of Medicine, Division of Endocrinology, University of California, Irvine, CA 92697, USA
Interests: cell cycle checkpoint control; DNA damage and repair pathway; Nek1 protein kinase; polycystic kidney disease; AKT and mitochondrial function
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondria play critical metabolic roles in fatty acid oxidation, the Krebs cycle, and oxidative phosphorylation. These processes generate reactive oxygen species (ROS), which are toxic to cells because they cause oxidative damage to mitochondrial lipids, DNA, and proteins. Damaged mitochondria also release high levels of Ca2+ and cytochrome C, inducing apoptosis.  To maintain the quality and quantity, selective autophagy—known as mitophagy—eliminates damaged mitochondria.

In addition to ROS-induced damage, alterations in mitochondrial function through mutations in either the mitochondrial or nuclear genome are associated with various diseases, including as cancer, aging, and metabolic disorders. The first evidence for mitochondrial involvement in cancer came from Warburg’s landmark observation that tumors produce excess lactate in the presence of oxygen, now known as the “Warburg effect”, a form of aerobic glycolysis. Activation of cellular signal transduction pathways, such as the PI3’K/PTEN/Akt pathway, also plays an important role in shifting metabolism from oxidative to glycolytic phosphorylation. Increasing evidence suggests that AKT kinase activity within mitochondria is crucial for cellular defense against extrinsic insults such as ischemia–reperfusion injury.

This Special Issue highlights diverse aspects of mitochondrial function in cancer, kidney disease, apoptosis, and autophagy, and further discusses the therapeutic potential of targeting mitochondria.

Dr. Yumay Chen
Guest Editor

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Keywords

  • mitochondial genesis and disease
  • mitochondrial function and aging
  • mitochondrial dysfunction and cancer
  • mitochondrial function and apoptosis
  • mitophage
  • autophage
  • mitochondrial AKT

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Published Papers (1 paper)

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Research

17 pages, 1337 KB  
Article
The Participation of Acetyl Phosphate, a Microbial and Host Metabolite, in the Regulation of the Calcium Balance in Mitochondria and Cells
by Natalia V. Beloborodova, Alexey V. Berezhnov and Nadezhda I. Fedotcheva
Int. J. Mol. Sci. 2026, 27(2), 1007; https://doi.org/10.3390/ijms27021007 - 20 Jan 2026
Viewed by 141
Abstract
Acetyl phosphate (AcP) is a microbial metabolite acting as a link between cell metabolism and signaling, providing the survival of bacteria in the host. AcP was also identified as an intermediate of pyruvate oxidation in mammalian mitochondria and was found in the human [...] Read more.
Acetyl phosphate (AcP) is a microbial metabolite acting as a link between cell metabolism and signaling, providing the survival of bacteria in the host. AcP was also identified as an intermediate of pyruvate oxidation in mammalian mitochondria and was found in the human blood in some severe pathologies. The possible contribution of circulating AcP to the maintenance of the physiological or pathological states of the body has not been studied. Since AcP can function as a donor of phosphate groups, we have examined in vitro the influence of AcP on calcium signaling in mitochondria and cells by measuring the membrane potential and the calcium retention capacity of mitochondria by selective electrodes and by assaying the cell calcium signaling by Fura-2AM fluorescent radiometry. AcP was shown to induce a concentration-dependent increase in the mitochondrial resistance to calcium ion loading both in the control and in the presence of ADP. This effect was especially pronounced when mitochondria were incubated in a phosphate-free medium; under these conditions, AcP strongly raised the membrane potential and increased the rate of calcium uptake and the calcium retention capacity several times. Moreover, AcP induced similar changes in human cells when calcium signaling was activated by ATP, to a greater extent in neuroblastoma cells than in astrocytes. In the presence of AcP, a tendency for an increase in the amplitude and a decrease in the continuance of the ATP-induced calcium response was observed. These changes are probably associated with the activation of calcium buffering by mitochondria due to the delivery of phosphate during the hydrolysis of AcP. The results show that AcP is involved in the regulation of the Ca2+ balance in cells by activating the accumulation of calcium ions by mitochondria, especially under phosphate deficiency. A shift in calcium signaling mediated by AcP supplementation may be caused by hyperphosphatemia, which is now considered as one of basic contributors to cellular dysfunction and progression of various diseases, including sepsis. Full article
(This article belongs to the Special Issue Mitochondrial Function in Human Health and Disease: 3rd Edition)
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