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Mitochondrial Functions and Dynamics

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: 30 September 2025 | Viewed by 690

Special Issue Editor


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Guest Editor
Department of Biomedical Sciences, Cittadella Universitaria di Monserrato, Monserrato, Italy
Interests: bioenergetics; ultrastructural morphology; mitochondrial cristae; morphometry; cell biology; HRSEM; TEM; protein expression

Special Issue Information

Dear Colleagues,

It has become increasingly evident that mitochondria play a role far beyond their traditional designation as the powerhouses of the cell. Indeed, mitochondria serve as the second most important calcium reservoir in cells, capable of exchanging calcium with the endoplasmic reticulum. Mitochondria are involved in oxidative stress, redox regulation, apoptosis, and aging. They integrate intracellular signals, contributing to the coordination of cellular functions. Recent studies have highlighted that mitochondria can be exchanged between different cell types and can even be found circulating in the bloodstream. Their role in immunomodulation, particularly concerning complex II (CII) activity, has emerged. Portions of mitochondria, or even mitochondrial DNA (mtDNA), can be released by one cell and taken up by neighboring cells. Moreover, the relationship between mitochondrial cristal shape and bioenergetic function presents another intriguing challenge for scientists. Exploring these various topics could lead to breakthroughs in addressing a range of pathological conditions associated with mitochondrial dysfunction.

We invite authors to submit articles on recent findings regarding the biochemical and molecular mechanisms of mitochondrial functions. Topics include mitochondrial biogenesis, bioenergetics, apoptosis, mitophagy, reactive oxygen species, calcium homeostasis, interactions with other organelles, and the link between mitochondrial dysfunction and cellular pathophysiology. Computational studies are also welcome.

Dr. Raffaella Isola
Guest Editor

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Keywords

  • bioenergetics
  • mitochondrial biogenesis
  • mitochondrial morphology
  • apoptosis
  • mitophagy
  • reactive oxygen species
  • calcium homeostasis
  • cardiovascular diseases
  • neurodegenerative diseases
  • in vitro, cellular, and animal models
  • myopathies
  • mitochondria and immune system

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Published Papers (1 paper)

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Research

22 pages, 31542 KiB  
Article
Pyrroloquinoline Quinone (PQQ) Attenuates Hydrogen Peroxide-Induced Injury Through the Enhancement of Mitochondrial Function in Human Trabecular Meshwork Cells
by Sabrina Petricca, Antonio Matrone, Daria Capece, Irene Flati, Vincenzo Flati, Enrico Ricevuto, Giuseppe Celenza, Nicola Franceschini, Mirco Mastrangelo, Cristina Pellegrini, Loredana Cristiano, Giuseppe Familiari, Benedetta Cinque, Giovanna Di Emidio, Carla Tatone and Roberto Iorio
Int. J. Mol. Sci. 2025, 26(14), 6938; https://doi.org/10.3390/ijms26146938 - 19 Jul 2025
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Abstract
Mitochondrial metabolism in the trabecular meshwork (TM) plays a critical role in maintaining intraocular pressure homeostasis by supporting the energy-demanding processes involved in aqueous humour outflow. In primary open-angle glaucoma, oxidative stress impairs mitochondrial function, leading to TM dysfunction. Therefore, understanding and targeting [...] Read more.
Mitochondrial metabolism in the trabecular meshwork (TM) plays a critical role in maintaining intraocular pressure homeostasis by supporting the energy-demanding processes involved in aqueous humour outflow. In primary open-angle glaucoma, oxidative stress impairs mitochondrial function, leading to TM dysfunction. Therefore, understanding and targeting mitochondrial health in TM cells could offer a novel therapeutic strategy. Pyrroloquinoline quinone (PQQ) is a redox cofactor with antioxidant and mitochondrial-enhancing properties. However, its effects on human TM (HTM) cells remain largely unexplored. This study examined PQQ cytoprotective effects against H2O2-induced oxidative stress in HTM cells. Seahorse analyses revealed that PQQ alone improves mitochondrial respiration and ATP production. Moreover, PQQ mitigates H2O2-induced cellular damage and preserves mitochondrial function by normalising proton leak and increasing ATP levels. Furthermore, TEM and confocal microscopy showed that PQQ can partially alleviate structural damage, restoring mitochondrial network morphology, thereby leading to reduced cell death. Although these protective effects seem not to be mediated by changes in mitochondrial content or activation of the SIRT1/PGC1-α pathway, they may involve modulation of SIRT3, a key factor of mitochondrial metabolism and homeostasis. Overall, these results suggest that PQQ may represent a promising candidate for restoring mitochondrial function and reversing oxidative damage in HTM cells. Full article
(This article belongs to the Special Issue Mitochondrial Functions and Dynamics)
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