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Life
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Mitochondrial Function and Signaling to Regulate Cellular Life
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Mitochondrial Function and Signaling to Regulate Cellular Life

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Cell Biology and Tissue Engineering".

Deadline for manuscript submissions: closed (31 January 2023) | Viewed by 37637

Special Issue Editors

Dr. Rafael A. Casuso

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Guest Editor
Department of Physiology, Institute of Nutrition and Food Technology, University of Granada, 18010 Granada, Spain
Interests: mitochondria; oxidative stress; exercise physiology; skeletal muscle
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Christian Cortés-Rojo

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Co-Guest Editor
Instituto de Investigaciones Químico-Biológicas, Universidad Michoacana de San Nicolás de Hidalgo, Morelia, Michoacán, México
Interests: mitochondrial dysfunction in chronic degenerative diseases; functional foods and nutraceuticals in oxidative stress; inflammation and mitochondrial dysfunction in chronic degenerative diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The primary role of mitochondria is to supply ATP to the cell; however, these organelles are also signaling hubs which receive and transmit signals to and from most cellular compartments. The importance of mitochondria in living cells is illustrated by the fact that severe mitochondrial stress can result in cellular apoptosis. Therefore, mitochondria have evolved to adapt in order to properly maintain cellular function under stressful environments. In this regard, mitochondria undergo a cell-like cycle where dysfunctional parts are separated through fission in order to be removed by the lysosome. Additionally, mitochondria are constantly synthesized (biogenesis) in a mechanism coordinated by both the nuclear and the mitochondrial genome, which are in constant crosstalk. Therefore, understanding the mitochondrial response to stress and the molecular mechanisms that enhance mitochondrial function will be of great value to prevent and reverse a variety of age-related metabolic diseases.

Dr. Rafael A. Casuso
Prof. Dr. Christian Cortés-Rojo
Guest Editors

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Keywords

  • mitochondrial function 
  • exercise 
  • nutrition 
  • reactive oxygen species 
  • electron transport chain 
  • metabolic disease

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Related Special Issue

Published Papers (11 papers)

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Editorial

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3 pages, 183 KiB  
Editorial
Mitochondrial Function and Signaling to Regulate Cellular Life
by Rafael A. Casuso
Life 2023, 13(4), 975; https://doi.org/10.3390/life13040975 - 9 Apr 2023
Viewed by 1402
Abstract
Mitochondria are essential organelles found in nearly all eukaryotic cells, responsible for producing the energy that drives cellular processes [...] Full article
(This article belongs to the Special Issue Mitochondrial Function and Signaling to Regulate Cellular Life)

Research

Jump to: Editorial, Review

15 pages, 1667 KiB  
Article
Isolated Mitochondria State after Myocardial Ischemia-Reperfusion Injury and Cardioprotection: Analysis by Flow Cytometry
by Claire Crola Da Silva, Delphine Baetz, Marie Védère, Mégane Lo-Grasso, Mariam Wehbi, Christophe Chouabe, Gabriel Bidaux and René Ferrera
Life 2023, 13(3), 707; https://doi.org/10.3390/life13030707 - 6 Mar 2023
Cited by 4 | Viewed by 2154
Abstract
Rationale: Mitochondria are key organelles involved in cell survival and death during the acute phenomena of myocardial ischemia-reperfusion (i.e., myocardial infarction). To investigate the functions of isolated mitochondria such as calcium retention capacity, oxidative phosphorylation, and reactive oxygen species (ROS) production, already established [...] Read more.
Rationale: Mitochondria are key organelles involved in cell survival and death during the acute phenomena of myocardial ischemia-reperfusion (i.e., myocardial infarction). To investigate the functions of isolated mitochondria such as calcium retention capacity, oxidative phosphorylation, and reactive oxygen species (ROS) production, already established methods are based on extramitochondrial measurements of the whole mitochondria population. Objective: The aim of this study was to develop a reliable and well-characterized method for multiparametric analysis of isolated single mitochondrion by flow cytometry (FC) in the context of myocardial infarction. The advantage of FC is the possibility to give a simultaneous analysis of morphological parameters (side and forward scatters: SSC and FSC) for each mitochondrion, combined with intramitochondrial measurements of several biological markers, such as ROS production or membrane potential (Δφm), using specific fluorescent probes. Methods and Results: For this study, a rat model of ischemia-reperfusion and a protective approach of post-conditioning using low reperfusion pressure was used. Thanks to the use of specific probes (NAO, MTR, TMRM, DilC1, and DHR123) combined with flow cytometry, we propose a method: (i) to identify mitochondrial populations of interest based on quality criteria (NAO/TMRM double staining); (ii) to monitor their morphological criteria, especially during swelling due to calcium overload; and (iii) to compare mitochondrial functions (membrane potential and ROS production) in different experimental groups. Applied to mitochondria from ischemic hearts, these measurements revealed that individual mitochondria are altered and that cardioprotection by low-pressure reperfusion reduces damage, as expected. Conclusions: Our results highlight FC as a reliable and sensitive method to investigate changes in mitochondrial functions and morphology in pathological conditions that disrupts their activity such as the case in ischemia-reperfusion. This methodological approach can be extended to other pathologies involving mitochondrial dysfunctions. Moreover, FC offers the possibility to work with very small amounts of isolated mitochondria, a factor that may limit the use of classical methods. Full article
(This article belongs to the Special Issue Mitochondrial Function and Signaling to Regulate Cellular Life)
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19 pages, 2350 KiB  
Article
Increased Mitochondrial Calcium Fluxes in Hypertrophic Right Ventricular Cardiomyocytes from a Rat Model of Pulmonary Artery Hypertension
by Anna Maria Krstic, Amelia S. Power and Marie-Louise Ward
Life 2023, 13(2), 540; https://doi.org/10.3390/life13020540 - 15 Feb 2023
Cited by 2 | Viewed by 2295
Abstract
Pulmonary artery hypertension causes right ventricular hypertrophy which rapidly progresses to heart failure with underlying cardiac mitochondrial dysfunction. Prior to failure, there are alterations in cytosolic Ca2+ handling that might impact mitochondrial function in the compensatory phase of RV hypertrophy. Our aims, [...] Read more.
Pulmonary artery hypertension causes right ventricular hypertrophy which rapidly progresses to heart failure with underlying cardiac mitochondrial dysfunction. Prior to failure, there are alterations in cytosolic Ca2+ handling that might impact mitochondrial function in the compensatory phase of RV hypertrophy. Our aims, therefore, were (i) to measure beat-to-beat mitochondrial Ca2+ fluxes, and (ii) to determine mitochondrial abundance and function in non-failing, hypertrophic cardiomyocytes. Male Wistar rats were injected with either saline (CON) or monocrotaline (MCT) to induce pulmonary artery hypertension and RV hypertrophy after four weeks. Cytosolic Ca2+ ([Ca2+]cyto) transients were obtained in isolated right ventricular (RV) cardiomyocytes, and mitochondrial Ca2+ ([Ca2+]mito) was recorded in separate RV cardiomyocytes. The distribution and abundance of key proteins was determined using confocal and stimulated emission depletion (STED) microscopy. The RV mitochondrial function was also assessed in RV homogenates using oxygraphy. The MCT cardiomyocytes had increased area, larger [Ca2+]cyto transients, increased Ca2+ store content, and faster trans-sarcolemmal Ca2+ extrusion relative to CON. The MCT cardiomyocytes also had larger [Ca2+]mito transients. STED images detected increased mitochondrial protein abundance (TOM20 clusters per μm2) in MCT, yet no difference was found when comparing mitochondrial respiration and membrane potential between the groups. We suggest that the larger [Ca2+]mito transients compensate to match ATP supply to the increased energy demands of hypertrophic cardiomyocytes. Full article
(This article belongs to the Special Issue Mitochondrial Function and Signaling to Regulate Cellular Life)
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12 pages, 2130 KiB  
Article
Linolenic Acid Plus Ethanol Exacerbates Cell Death in Saccharomyces cerevisiae by Promoting Lipid Peroxidation, Cardiolipin Loss, and Necrosis
by Berenice Eridani Olmos-Orizaba, José Santos Arroyo-Peñaloza, Lorena Martínez-Alcántar, Rocío Montoya-Pérez, Alberto Flores-García, Alain Raimundo Rodríguez-Orozco, Elizabeth Calderón-Cortés, Alfredo Saavedra-Molina, Jesús Campos-García and Christian Cortés-Rojo
Life 2022, 12(7), 1052; https://doi.org/10.3390/life12071052 - 14 Jul 2022
Cited by 5 | Viewed by 1865
Abstract
Polyunsaturated fatty acids (PUFA) hypersensitize yeast to oxidative stress. Ethanol accumulation during fermentation is another factor that induces oxidative stress via mitochondrial dysfunction and ROS overproduction. Since this microorganism has raised growing interest as a PUFA factory, we have studied if the combination [...] Read more.
Polyunsaturated fatty acids (PUFA) hypersensitize yeast to oxidative stress. Ethanol accumulation during fermentation is another factor that induces oxidative stress via mitochondrial dysfunction and ROS overproduction. Since this microorganism has raised growing interest as a PUFA factory, we have studied if the combination of PUFA plus ethanol enhances yeast death. Respiration, ROS generation, lipid peroxidation, mitochondrial cardiolipin content, and cell death were assessed in yeast grown in the presence of 10% ethanol (ETOH) or linolenic acid (C18:3), or ethanol plus C18:3 (ETOH+C18:3). Lipid peroxidation and cardiolipin loss were several-fold higher in cells with ETOH+C18:3 than with C18:3. On the contrary, ETOH tended to increase cardiolipin content without inducing changes in lipid peroxidation. This was consistent with a remarkable diminution of cell growth and an exacerbated propidium iodide staining in cells with only ETOH+C18:3. The respiration rate decreased with all the treatments to a similar degree, and this was paralleled with similar increments in ROS between all the treatments. These results indicate that PUFA plus ethanol hypersensitize yeast to necrotic cell death by exacerbating membrane damage and mitochondrial cardiolipin loss, independent of mitochondrial dysfunction and ROS generation. The implications of these observations for some biotechnological applications in yeast and its physiology are discussed. Full article
(This article belongs to the Special Issue Mitochondrial Function and Signaling to Regulate Cellular Life)
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18 pages, 1494 KiB  
Article
Protection against Osteoarthritis Symptoms by Aerobic Exercise with a High-Protein Diet by Reducing Inflammation in a Testosterone-Deficient Animal Model
by Sunmin Park, Suna Kang, Da Sol Kim and Ting Zhang
Life 2022, 12(2), 177; https://doi.org/10.3390/life12020177 - 26 Jan 2022
Cited by 5 | Viewed by 3218
Abstract
A testosterone deficiency potentially increases osteoarthritis (OA) symptoms, and dietary protein and exercise affect them. However, their efficacy and their interactions are still unclear. We hypothesized that a high-protein diet (HPD) and regular exercise modulated OA symptoms in testosterone-deficient rats, and it was [...] Read more.
A testosterone deficiency potentially increases osteoarthritis (OA) symptoms, and dietary protein and exercise affect them. However, their efficacy and their interactions are still unclear. We hypothesized that a high-protein diet (HPD) and regular exercise modulated OA symptoms in testosterone-deficient rats, and it was examined in bilateral orchidectomized (ORX) and monoiodoacetate (MIA)-injected rats. The ORX rats were given a 30 energy percent (En%) protein (HPD) or 17.5 En% protein (CD). Both groups had 39 En% fat in the diet. Non-ORX-CD rats (sham-operation of ORX) were given the CD and no exercise (normal control). After an eight-week intervention, all rats had an injection of MIA into the left knee, and the treatments were continued for an additional four weeks. The non-ORX-CD rats showed a significant increase in body weight compared to the ORX rats, but the ORX rats had elevated fat mass. ORX exacerbated the glucose tolerance by lowering the serum insulin concentrations and increasing insulin resistance. ORX exacerbated the OA symptoms more than the non-ORX-CD. The HPD and exercise improved bone mineral density and glucose metabolism without changing serum testosterone concentrations, while only exercise increased the lean body mass and decreased fat mass, lipid peroxide, and inflammation. Exercise, but not HPD, reduced the OA symptoms, the weight distribution in the left leg, and running velocity and provided better relief than the non-ORX-CD rats. Exercise with HPD improved the histology of the knee joint in the left leg. Exercise reduced lipid peroxide contents and TNF-α and IL-1β mRNA expression in the articular cartilage, while exercise with HPD decreased MMP-3 and MMP-13 mRNA expression as much as in the non-ORX-CD group. In conclusion, moderate aerobic exercise with HPD alleviated OA symptoms and articular cartilage degradation in a similar way in the non-ORX rats with OA by alleviating inflammation and oxidative stress. Full article
(This article belongs to the Special Issue Mitochondrial Function and Signaling to Regulate Cellular Life)
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9 pages, 745 KiB  
Article
Physiological Doses of Hydroxytyrosol Modulate Gene Expression in Skeletal Muscle of Exercised Rats
by Rafael A. Casuso, Saad Al Fazazi, Julio Plaza-Díaz, Francisco J. Ruiz-Ojeda, Ascensión Rueda-Robles, Jerónimo Aragón-Vela and Jesús R. Huertas
Life 2021, 11(12), 1393; https://doi.org/10.3390/life11121393 - 12 Dec 2021
Cited by 2 | Viewed by 2823
Abstract
We tested whether physiological doses of hydroxytyrosol (HT) may alter the mRNA transcription of key metabolic genes in exercised skeletal muscle. Two groups of exercise-trained Wistar rats, HTlow and HTmid, were supplemented with 0.31 and 4.61 mg/kg/d of HT, respectively, for 10 weeks. [...] Read more.
We tested whether physiological doses of hydroxytyrosol (HT) may alter the mRNA transcription of key metabolic genes in exercised skeletal muscle. Two groups of exercise-trained Wistar rats, HTlow and HTmid, were supplemented with 0.31 and 4.61 mg/kg/d of HT, respectively, for 10 weeks. Another two groups of rats were not supplemented with HT; one remained sedentary and the other one was exercised. After the experimental period, the soleus muscle was removed for qRT-PCR and western blot analysis. The consumption of 4.61 mg/kg/d of HT during exercise increased the mRNA expression of important metabolic proteins. Specifically, 4.61 mg/kg/d of HT may upregulate long-chain fatty acid oxidation, lactate, and glucose oxidation as well as mitochondrial Krebs cycle in trained skeletal muscle. However, a 4.61 mg/kg/d of HT may alter protein translation, as in spite of the increment showed by CD36 and GLUT4 at the mRNA level this was not translated to higher protein content. Full article
(This article belongs to the Special Issue Mitochondrial Function and Signaling to Regulate Cellular Life)
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13 pages, 2865 KiB  
Article
Coupling/Uncoupling Reversibility in Isolated Mitochondria from Saccharomyces cerevisiae
by Lilia Morales-García, Carolina Ricardez-García, Paulina Castañeda-Tamez, Natalia Chiquete-Félix and Salvador Uribe-Carvajal
Life 2021, 11(12), 1307; https://doi.org/10.3390/life11121307 - 27 Nov 2021
Cited by 6 | Viewed by 2387
Abstract
The yeast Saccharomyces cerevisiae uses fermentation as the preferred pathway to obtain ATP and requires the respiratory chain to re-oxidize the NADH needed for activity of Glyceraldehyde-3-phosphate. This process is favored by uncoupling of oxidative phosphorylation (OxPhos), which is at least partially controlled [...] Read more.
The yeast Saccharomyces cerevisiae uses fermentation as the preferred pathway to obtain ATP and requires the respiratory chain to re-oxidize the NADH needed for activity of Glyceraldehyde-3-phosphate. This process is favored by uncoupling of oxidative phosphorylation (OxPhos), which is at least partially controlled by the mitochondrial unspecific pore (ScMUC). When mitochondrial ATP synthesis is needed as in the diauxic phase or during mating, a large rise in Ca2+ concentration ([Ca2+]) closes ScMUC, coupling OxPhos. In addition, ScMUC opening/closing is mediated by the ATP/ADP ratio, which indicates cellular energy needs. Here, opening and closing of ScMUC was evaluated in isolated mitochondria from S. cerevisiae at different incubation times and in the presence of different ATP/ADP ratios or varying [Ca2+]. Measurements of the rate of O2 consumption, mitochondrial swelling, transmembrane potential and ROS generation were conducted. It was observed that ScMUC opening was reversible, a high ATP/ADP ratio promoted opening and [Ca2+] closed ScMUC even after several minutes of incubation in the open state. In the absence of ATP synthesis, closure of ScMUC resulted in an increase in ROS. Full article
(This article belongs to the Special Issue Mitochondrial Function and Signaling to Regulate Cellular Life)
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13 pages, 3870 KiB  
Article
Avocado Oil Prevents Kidney Injury and Normalizes Renal Vasodilation after Adrenergic Stimulation in Hypertensive Rats: Probable Role of Improvement in Mitochondrial Dysfunction and Oxidative Stress
by Cristian Adrián Márquez-Ramírez, Berenice Eridani Olmos-Orizaba, Claudia Isabel García-Berumen, Elizabeth Calderón-Cortés, Rocío Montoya-Pérez, Alfredo Saavedra-Molina, Alain Raimundo Rodríguez-Orozco and Christian Cortés-Rojo
Life 2021, 11(11), 1122; https://doi.org/10.3390/life11111122 - 21 Oct 2021
Cited by 5 | Viewed by 2661
Abstract
Hypertension impairs the function of the kidney and its vasculature. Adrenergic activation is involved in these processes by promoting oxidative stress and mitochondrial dysfunction. Thus, the targeting of mitochondrial function and mitochondrial oxidative stress may be an approach to alleviate hypertensive kidney damage. [...] Read more.
Hypertension impairs the function of the kidney and its vasculature. Adrenergic activation is involved in these processes by promoting oxidative stress and mitochondrial dysfunction. Thus, the targeting of mitochondrial function and mitochondrial oxidative stress may be an approach to alleviate hypertensive kidney damage. Avocado oil, a source of oleic acid and antioxidants, improves mitochondrial dysfunction, decreases mitochondrial oxidative stress, and enhances vascular function in hypertensive rats. However, whether avocado oil improves the function of renal vasculature during the adrenergic stimulation, and if this is related to improvement in renal damage and enhancement of mitochondrial activity is unknown. Thus, the effects of avocado oil on renal vascular responses to adrenergic stimulation, mitochondrial dysfunction, oxidative stress, and renal damage were compared with prazosin, an antagonist of α1-adrenoceptors, in hypertensive rats induced by L-NAME. Avocado oil or prazosin decreased blood pressure, improved endothelium—dependent renal vasodilation, prevented mitochondrial dysfunction and kidney damage in hypertensive rats. However, avocado oil, but not prazosin, decreased mitochondrial ROS generation and improved the redox state of mitochondrial glutathione. These results suggest that avocado oil and prazosin prevented hypertensive renal damage due to the improvement in mitochondrial function. Full article
(This article belongs to the Special Issue Mitochondrial Function and Signaling to Regulate Cellular Life)
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Review

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20 pages, 4637 KiB  
Review
From the Structural and (Dys)Function of ATP Synthase to Deficiency in Age-Related Diseases
by Caterina Garone, Andrea Pietra and Salvatore Nesci
Life 2022, 12(3), 401; https://doi.org/10.3390/life12030401 - 10 Mar 2022
Cited by 14 | Viewed by 4901
Abstract
The ATP synthase is a mitochondrial inner membrane complex whose function is essential for cell bioenergy, being responsible for the conversion of ADP into ATP and playing a role in mitochondrial cristae morphology organization. The enzyme is composed of 18 protein subunits, 16 [...] Read more.
The ATP synthase is a mitochondrial inner membrane complex whose function is essential for cell bioenergy, being responsible for the conversion of ADP into ATP and playing a role in mitochondrial cristae morphology organization. The enzyme is composed of 18 protein subunits, 16 nuclear DNA (nDNA) encoded and two mitochondrial DNA (mtDNA) encoded, organized in two domains, FO and F1. Pathogenetic variants in genes encoding structural subunits or assembly factors are responsible for fatal human diseases. Emerging evidence also underlines the role of ATP-synthase in neurodegenerative diseases as Parkinson’s, Alzheimer’s, and motor neuron diseases such as Amyotrophic Lateral Sclerosis. Post-translational modification, epigenetic modulation of ATP gene expression and protein level, and the mechanism of mitochondrial transition pore have been deemed responsible for neuronal cell death in vivo and in vitro models for neurodegenerative diseases. In this review, we will explore ATP synthase assembly and function in physiological and pathological conditions by referring to the recent cryo-EM studies and by exploring human disease models. Full article
(This article belongs to the Special Issue Mitochondrial Function and Signaling to Regulate Cellular Life)
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24 pages, 16495 KiB  
Review
Oxidative Stress, Mitochondrial Function and Adaptation to Exercise: New Perspectives in Nutrition
by Nancy Vargas-Mendoza, Marcelo Angeles-Valencia, Ángel Morales-González, Eduardo Osiris Madrigal-Santillán, Mauricio Morales-Martínez, Eduardo Madrigal-Bujaidar, Isela Álvarez-González, José Gutiérrez-Salinas, César Esquivel-Chirino, Germán Chamorro-Cevallos, José Melesio Cristóbal-Luna and José A. Morales-González
Life 2021, 11(11), 1269; https://doi.org/10.3390/life11111269 - 22 Nov 2021
Cited by 37 | Viewed by 6744
Abstract
Cells have the ability to adapt to stressful environments as a part of their evolution. Physical exercise induces an increase of a demand for energy that must be met by mitochondria as the main (ATP) provider. However, this process leads to the increase [...] Read more.
Cells have the ability to adapt to stressful environments as a part of their evolution. Physical exercise induces an increase of a demand for energy that must be met by mitochondria as the main (ATP) provider. However, this process leads to the increase of free radicals and the so-called reactive oxygen species (ROS), which are necessary for the maintenance of cell signaling and homeostasis. In addition, mitochondrial biogenesis is influenced by exercise in continuous crosstalk between the mitochondria and the nuclear genome. Excessive workloads may induce severe mitochondrial stress, resulting in oxidative damage. In this regard, the objective of this work was to provide a general overview of the molecular mechanisms involved in mitochondrial adaptation during exercise and to understand if some nutrients such as antioxidants may be implicated in blunt adaptation and/or an impact on the performance of exercise by different means. Full article
(This article belongs to the Special Issue Mitochondrial Function and Signaling to Regulate Cellular Life)
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36 pages, 4325 KiB  
Review
Mitochondrial Quality Control in Cardiac-Conditioning Strategies against Ischemia-Reperfusion Injury
by Wylly Ramsés García-Niño, Cecilia Zazueta, Mabel Buelna-Chontal and Alejandro Silva-Palacios
Life 2021, 11(11), 1123; https://doi.org/10.3390/life11111123 - 21 Oct 2021
Cited by 24 | Viewed by 5285
Abstract
Mitochondria are the central target of ischemic preconditioning and postconditioning cardioprotective strategies, which consist of either the application of brief intermittent ischemia/reperfusion (I/R) cycles or the administration of pharmacological agents. Such strategies reduce cardiac I/R injury by activating protective signaling pathways that prevent [...] Read more.
Mitochondria are the central target of ischemic preconditioning and postconditioning cardioprotective strategies, which consist of either the application of brief intermittent ischemia/reperfusion (I/R) cycles or the administration of pharmacological agents. Such strategies reduce cardiac I/R injury by activating protective signaling pathways that prevent the exacerbated production of reactive oxygen/nitrogen species, inhibit opening of mitochondrial permeability transition pore and reduce apoptosis, maintaining normal mitochondrial function. Cardioprotection also involves the activation of mitochondrial quality control (MQC) processes, which replace defective mitochondria or eliminate mitochondrial debris, preserving the structure and function of the network of these organelles, and consequently ensuring homeostasis and survival of cardiomyocytes. Such processes include mitochondrial biogenesis, fission, fusion, mitophagy and mitochondrial-controlled cell death. This review updates recent advances in MQC mechanisms that are activated in the protection conferred by different cardiac conditioning interventions. Furthermore, the role of extracellular vesicles in mitochondrial protection and turnover of these organelles will be discussed. It is concluded that modulation of MQC mechanisms and recognition of mitochondrial targets could provide a potential and selective therapeutic approach for I/R-induced mitochondrial dysfunction. Full article
(This article belongs to the Special Issue Mitochondrial Function and Signaling to Regulate Cellular Life)
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