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Mitochondrial Respiration in Physiology and Pathology
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Mitochondrial Respiration in Physiology and Pathology

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (14 July 2023) | Viewed by 16426

Special Issue Editors

Dr. Angela Anna Messina

E-Mail Website
Guest Editor
Department of Biological, Geological and Environmental Sciences, Section of Biochemistry and Molecular Biology, University of Catania, 95125 Catania, Italy
Interests: mitochondria; membrane proteins; bioenergetics; apoptosis; sequencing; protein–protein interaction; cell culture; recombinant protein expression
Special Issues, Collections and Topics in MDPI journals
Dr. Andrea Magrì

E-Mail Website
Guest Editor
Department of Biological, Geological and Environmental Sciences, University of Catania Via S. Sofia, 64 - Cittadella Universitaria Building 2, 95125 Catania, Italy
Interests: mitochondria; VDAC; porins; electrophysiology; planar lipid bilayer; high-resolution respirometry; mitochondrial dysfunction; als

Special Issue Information

Dear Colleagues,

Mitochondria are key organelles within the cell, regulating a variety of functions essential for the maintenance of cellular homeostasis. Beyond their involvement in apoptosis regulation pathways, their main mitochondrial function is to produce ATP via oxidative phosphorylation. In this perspective, oxygen consumption represents one of the most informative parameters for the evaluation of overall organelle functionality. Mitochondrial dysfunction is indeed generally associated with many pathologies, including cancer, diabetes, viral infections, and neurodegenerative disorders (such as Parkinson’s and Alzheimer’s diseases). The recent development of high-resolution and high-sensitive oxygraphy-based techniques has brought back respirometry as the gold standard for the determination of mitochondrial functionality in a wide range of conditions. The aim of this issue is to collect recent studies investigating mitochondrial function in physiological and/or pathological conditions. The deep understanding of specific mechanisms behind electron transport chains and OXPHOS malfunctioning is particularly important because of the potential development of any pharmacological strategy aimed at recovering the organelle function.

Dr. Angela Anna Messina
Dr. Andrea Magrì
Guest Editors

Manuscript Submission Information

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Keywords

  • mitochondria
  • mitochondrial function
  • ATP
  • organelles
  • cancer
  • diabetes
  • viral infections and neurodegenerative disorders
  • high-resolution and high-sensitive oxygraphy-based techniques

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Published Papers (7 papers)

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Editorial

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2 pages, 179 KiB  
Editorial
Special Issue “Mitochondrial Respiration in Physiology and Pathology”
by Angela Messina and Andrea Magrì
Int. J. Mol. Sci. 2024, 25(5), 2958; https://doi.org/10.3390/ijms25052958 - 3 Mar 2024
Viewed by 869
Abstract
Mitochondria are key organelles that regulate several functions essential for maintaining cellular homeostasis [...] Full article
(This article belongs to the Special Issue Mitochondrial Respiration in Physiology and Pathology)

Research

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18 pages, 3816 KiB  
Article
Mitochondrial sAC-cAMP-PKA Axis Modulates the ΔΨm-Dependent Control Coefficients of the Respiratory Chain Complexes: Evidence of Respirasome Plasticity
by Rosella Scrima, Olga Cela, Michela Rosiello, Ari Qadir Nabi, Claudia Piccoli, Giuseppe Capitanio, Francesco Antonio Tucci, Aldo Leone, Giovanni Quarato and Nazzareno Capitanio
Int. J. Mol. Sci. 2023, 24(20), 15144; https://doi.org/10.3390/ijms242015144 - 13 Oct 2023
Cited by 3 | Viewed by 1347
Abstract
The current view of the mitochondrial respiratory chain complexes I, III and IV foresees the occurrence of their assembly in supercomplexes, providing additional functional properties when compared with randomly colliding isolated complexes. According to the plasticity model, the two structural states of the [...] Read more.
The current view of the mitochondrial respiratory chain complexes I, III and IV foresees the occurrence of their assembly in supercomplexes, providing additional functional properties when compared with randomly colliding isolated complexes. According to the plasticity model, the two structural states of the respiratory chain may interconvert, influenced by the intracellular prevailing conditions. In previous studies, we suggested the mitochondrial membrane potential as a factor for controlling their dynamic balance. Here, we investigated if and how the cAMP/PKA-mediated signalling influences the aggregation state of the respiratory complexes. An analysis of the inhibitory titration profiles of the endogenous oxygen consumption rates in intact HepG2 cells with specific inhibitors of the respiratory complexes was performed to quantify, in the framework of the metabolic flux theory, the corresponding control coefficients. The attained results, pharmacologically inhibiting either PKA or sAC, indicated that the reversible phosphorylation of the respiratory chain complexes/supercomplexes influenced their assembly state in response to the membrane potential. This conclusion was supported by the scrutiny of the available structure of the CI/CIII2/CIV respirasome, enabling us to map several PKA-targeted serine residues exposed to the matrix side of the complexes I, III and IV at the contact interfaces of the three complexes. Full article
(This article belongs to the Special Issue Mitochondrial Respiration in Physiology and Pathology)
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16 pages, 2666 KiB  
Article
VDAC1 Knockout Affects Mitochondrial Oxygen Consumption Triggering a Rearrangement of ETC by Impacting on Complex I Activity
by Andrea Magrì, Salvatore Antonio Maria Cubisino, Giuseppe Battiato, Cristiana Lucia Rita Lipari, Stefano Conti Nibali, Miriam Wissam Saab, Alessandra Pittalà, Angela Maria Amorini, Vito De Pinto and Angela Messina
Int. J. Mol. Sci. 2023, 24(4), 3687; https://doi.org/10.3390/ijms24043687 - 12 Feb 2023
Cited by 7 | Viewed by 2478
Abstract
Voltage-Dependent Anion-selective Channel isoform 1 (VDAC1) is the most abundant isoform of the outer mitochondrial membrane (OMM) porins and the principal gate for ions and metabolites to and from the organelle. VDAC1 is also involved in a number of additional functions, such as [...] Read more.
Voltage-Dependent Anion-selective Channel isoform 1 (VDAC1) is the most abundant isoform of the outer mitochondrial membrane (OMM) porins and the principal gate for ions and metabolites to and from the organelle. VDAC1 is also involved in a number of additional functions, such as the regulation of apoptosis. Although the protein is not directly involved in mitochondrial respiration, its deletion in yeast triggers a complete rewiring of the whole cell metabolism, with the inactivation of the main mitochondrial functions. In this work, we analyzed in detail the impact of VDAC1 knockout on mitochondrial respiration in the near-haploid human cell line HAP1. Results indicate that, despite the presence of other VDAC isoforms in the cell, the inactivation of VDAC1 correlates with a dramatic impairment in oxygen consumption and a re-organization of the relative contributions of the electron transport chain (ETC) enzymes. Precisely, in VDAC1 knockout HAP1 cells, the complex I-linked respiration (N-pathway) is increased by drawing resources from respiratory reserves. Overall, the data reported here strengthen the key role of VDAC1 as a general regulator of mitochondrial metabolism. Full article
(This article belongs to the Special Issue Mitochondrial Respiration in Physiology and Pathology)
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14 pages, 2319 KiB  
Article
Therapeutic Effect of Mitochondrial Division Inhibitor-1 (Mdivi-1) on Hyperglycemia-Exacerbated Early and Delayed Brain Injuries after Experimental Subarachnoid Hemorrhage
by Chia-Li Chung, Yu-Hua Huang, Chien-Ju Lin, Yoon-Bin Chong, Shu-Chuan Wu, Chee-Yin Chai, Hung-Pei Tsai and Aij-Lie Kwan
Int. J. Mol. Sci. 2022, 23(13), 6924; https://doi.org/10.3390/ijms23136924 - 22 Jun 2022
Cited by 8 | Viewed by 2316
Abstract
Background: Neurological deficits following subarachnoid hemorrhage (SAH) are caused by early or delayed brain injuries. Our previous studies have demonstrated that hyperglycemia induces profound neuronal apoptosis of the cerebral cortex. Morphologically, we found that hyperglycemia exacerbated late vasospasm following SAH. Thus, our previous [...] Read more.
Background: Neurological deficits following subarachnoid hemorrhage (SAH) are caused by early or delayed brain injuries. Our previous studies have demonstrated that hyperglycemia induces profound neuronal apoptosis of the cerebral cortex. Morphologically, we found that hyperglycemia exacerbated late vasospasm following SAH. Thus, our previous studies strongly suggest that post-SAH hyperglycemia is not only a response to primary insult, but also an aggravating factor for brain injuries. In addition, mitochondrial fusion and fission are vital to maintaining cellular functions. Current evidence also shows that the suppression of mitochondrial fission alleviates brain injuries after experimental SAH. Hence, this study aimed to determine the effects of mitochondrial dynamic modulation in hyperglycemia-related worse SAH neurological prognosis. Materials and methods: In vitro, we employed an enzyme-linked immunosorbent assay (ELISA) to detect the effect of mitochondrial division inhibitor-1 (Mdivi-1) on lipopolysaccharide (LPS)-induced BV-2 cells releasing inflammatory factors. In vivo, we produced hyperglycemic rats via intraperitoneal streptozotocin (STZ) injections. Hyperglycemia was confirmed using blood-glucose measurements (>300 mg/dL) 7 days after the STZ injection. The rodent model of SAH, in which fresh blood was instilled into the craniocervical junction, was used 7 days after STZ administration. We investigated the mechanism and effect of Mdivi-1, a selective inhibitor of dynamin-related protein (Drp1) to downregulate mitochondrial fission, on SAH-induced apoptosis in a hyperglycemic state, and evaluated the results in a dose–response manner. The rats were divided into the following five groups: (1) control, (2) SAH only, (3) Diabetes mellitus (DM) + SAH, (4) Mdivi-1 (0.24 mg/kg) + DM + SAH, and (5) Mdivi-1 (1.2 mg/kg) + DM + SAH. Results: In vitro, ELISA revealed that Mdivi-1 inhibited microglia from releasing inflammatory factors, such as tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6. In vivo, neurological outcomes in the high-dose (1.2 mg/kg) Mdivi-1 treatment group were significantly reduced compared with the SAH and DM + SAH groups. Furthermore, immunofluorescence staining and ELISA revealed that a high dose of Mdivi-1 had attenuated inflammation and neuron cell apoptosis by inhibiting Hyperglycemia-aggravated activation, as well as microglia and astrocyte proliferation, following SAH. Conclusion: Mdivi-1, a Drp-1 inhibitor, attenuates cerebral vasospasm, poor neurological outcomes, inflammation, and neuron cell apoptosis following SAH + hyperglycemia. Full article
(This article belongs to the Special Issue Mitochondrial Respiration in Physiology and Pathology)
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17 pages, 3486 KiB  
Article
Mitochondrial Side Effects of Surgical Prophylactic Antibiotics Ceftriaxone and Rifaximin Lead to Bowel Mucosal Damage
by Bálint Baráth, Dávid K. Jász, Tamara Horváth, Bence Baráth, Gergely Maróti, Gerda Strifler, Gabriella Varga, Lilla Sándor, Domonkos Perényi, Szabolcs Tallósy, Tibor Donka, Péter Jávor, Mihály Boros and Petra Hartmann
Int. J. Mol. Sci. 2022, 23(9), 5064; https://doi.org/10.3390/ijms23095064 - 3 May 2022
Cited by 3 | Viewed by 2927
Abstract
Despite their clinical effectiveness, a growing body of evidence has shown that many classes of antibiotics lead to mitochondrial dysfunction. Ceftriaxone and Rifaximin are first choice perioperative antibiotics in gastrointestinal surgery targeting fundamental processes of intestinal bacteria; however, may also have negative consequences [...] Read more.
Despite their clinical effectiveness, a growing body of evidence has shown that many classes of antibiotics lead to mitochondrial dysfunction. Ceftriaxone and Rifaximin are first choice perioperative antibiotics in gastrointestinal surgery targeting fundamental processes of intestinal bacteria; however, may also have negative consequences for the host cells. In this study, we investigated their direct effect on mitochondrial functions in vitro, together with their impact on ileum, colon and liver tissue. Additionally, their impact on the gastrointestinal microbiome was studied in vivo, in a rat model. Rifaximin significantly impaired the oxidative phosphorylation capacity (OxPhos) and leak respiration in the ileal mucosa, in line with increased oxidative tissue damage and histological changes following treatment. Ceftriaxone prophylaxis led to similar changes in the colon mucosa. The composition and diversity of bacterial communities differed extensively in response to antibiotic pre-treatment. However, the relative abundances of the toxin producing species were not increased. We have confirmed the harmful effects of prophylactic doses of Rifaximin and Ceftriaxone on the intestinal mucosa and that these effects were related to the mitochondrial dysfunction. These experiments raise awareness of mitochondrial side effects of these antibiotics that may be of clinical importance when evaluating their adverse effects on bowel mucosa. Full article
(This article belongs to the Special Issue Mitochondrial Respiration in Physiology and Pathology)
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16 pages, 2651 KiB  
Article
Gamma-Aminobutyrate Transaminase Protects against Lipid Overload-Triggered Cardiac Injury in Mice
by Mengxiao Zhang, Huiting Zhong, Ting Cao, Yifan Huang, Xiaoyun Ji, Guo-Chang Fan and Tianqing Peng
Int. J. Mol. Sci. 2022, 23(4), 2182; https://doi.org/10.3390/ijms23042182 - 16 Feb 2022
Cited by 9 | Viewed by 2566
Abstract
Lipid overload contributes to cardiac complications of diabetes and obesity. However, the underlying mechanisms remain obscure. This study investigates the role of gamma-aminobutyrate transaminase (ABAT), the key enzyme involved in the catabolism of γ-aminobutyric acid (GABA), in lipid overload-induced cardiac injury. Microarray revealed [...] Read more.
Lipid overload contributes to cardiac complications of diabetes and obesity. However, the underlying mechanisms remain obscure. This study investigates the role of gamma-aminobutyrate transaminase (ABAT), the key enzyme involved in the catabolism of γ-aminobutyric acid (GABA), in lipid overload-induced cardiac injury. Microarray revealed a down-regulation of ABAT mRNA expression in high fat diet (HFD)-fed mouse hearts, which correlated with a reduction in ABAT protein level and its GABA catabolic activity. Transgenic mice with cardiomyocyte-specific ABAT over-expression (Tg-ABAT/tTA) were generated to determine the role of ABAT in lipid overload-induced cardiac injury. Feeding with a HFD to control mice for 4 months reduced ATP production and the mitochondrial DNA copy number, and induced myocardial oxidative stress, hypertrophy, fibrosis and dysfunction. Such pathological effects of HFD were mitigated by ABAT over-expression in Tg-ABAT/tTA mice. In cultured cardiomyocytes, palmitate increased mitochondrial ROS production, depleted ATP production and promoted apoptosis, all of which were attenuated by ABAT over-expression. With the inhibition of ABAT’s GABA catabolic activity, the protective effects of ABAT remained unchanged in palmitate-induced cardiomyocytes. Thus, ABAT protects the mitochondrial function in defending the heart against lipid overload-induced injury through mechanisms independent of its GABA catabolic activity, and may represent a new therapeutic target for lipid overload-induced cardiac injury. Full article
(This article belongs to the Special Issue Mitochondrial Respiration in Physiology and Pathology)
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Review

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19 pages, 2017 KiB  
Review
Mitochondrial Dynamics and Insulin Secretion
by Uma D. Kabra and Martin Jastroch
Int. J. Mol. Sci. 2023, 24(18), 13782; https://doi.org/10.3390/ijms241813782 - 7 Sep 2023
Cited by 8 | Viewed by 2450
Abstract
Mitochondria are involved in the regulation of cellular energy metabolism, calcium homeostasis, and apoptosis. For mitochondrial quality control, dynamic processes, such as mitochondrial fission and fusion, are necessary to maintain shape and function. Disturbances of mitochondrial dynamics lead to dysfunctional mitochondria, which contribute [...] Read more.
Mitochondria are involved in the regulation of cellular energy metabolism, calcium homeostasis, and apoptosis. For mitochondrial quality control, dynamic processes, such as mitochondrial fission and fusion, are necessary to maintain shape and function. Disturbances of mitochondrial dynamics lead to dysfunctional mitochondria, which contribute to the development and progression of numerous diseases, including Type 2 Diabetes (T2D). Compelling evidence has been put forward that mitochondrial dynamics play a significant role in the metabolism-secretion coupling of pancreatic β cells. The disruption of mitochondrial dynamics is linked to defects in energy production and increased apoptosis, ultimately impairing insulin secretion and β cell death. This review provides an overview of molecular mechanisms controlling mitochondrial dynamics, their dysfunction in pancreatic β cells, and pharmaceutical agents targeting mitochondrial dynamic proteins, such as mitochondrial division inhibitor-1 (mdivi-1), dynasore, P110, and 15-oxospiramilactone (S3). Full article
(This article belongs to the Special Issue Mitochondrial Respiration in Physiology and Pathology)
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