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Targeted Protection of Bioactive Compounds to Mitochondria
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Targeted Protection of Bioactive Compounds to Mitochondria

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

Deadline for manuscript submissions: closed (31 October 2019) | Viewed by 43771

Special Issue Editors

Dr. Lillà Lionetti

E-Mail Website
Guest Editor
Department of Chemistry and Biology, University of Salerno, 84084 Fisciano, Italy
Interests: unsaturated fatty acids; hepatic steatosis; insulin resistance; mitochondrial function and dynamics; endocrine disruptors
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Assunta Lombardi

E-Mail Website
Guest Editor
Università degli Studi di Napoli Federico II, Department of Biology, Naples, Italy

Special Issue Information

Dear Colleagues,

Mitochondria play a key role in many cellular processes and can rapidly adapt to meet the metabolic needs of a cell in response to change in environmental condition. Their dysfunction has been related to metabolic disease associated with obesity, such as insulin resistance, diabetes, cardiovascular disease, cancer and neurodegenerative disease. It has been also shown that mitochondrial function is strictly related to their dynamic behaviour in terms of balance of fusion and fission processes. Mitochondrial impairment results in the removal of damaged mitochondria through fission and mitophagy, whereas the fusion of individual mitochondria into dynamic network is associated with improvement of mitochondrial function.

This Special Issue is focused on the protective effects of bioactive compounds on mitochondrial bioenergetics and dynamic behaviour. Different bioactive compounds have been shown to improve mitochondrial function and dynamic behaviour, counteracting cellular damage, tissue dysfunction and metabolic diseases. The submission of original research articles or reviews related to the targeted protection of bioactive compounds to mitochondria is encouraged. It is particularly encouraged the submission of manuscript focused on clarify at the cellular and molecular level, the role of bioactive compounds in regulating interaction between mitochondria and the others intracellular components, such as endoplasmic reticulum and nucleus, as well as their impact into the interplay between mitochondrial bioenergetics, reactive oxygen species production and inflammatory pathways in the frame of the new concept of metaflammasome. Understanding how bioactive compounds may improve mitochondrial bioenergetics and metabolic adaptation at the cellular and molecular level, has the potential to generate new knowledge that will lead to improved treatment or protection towards many of the metabolic diseases that characterize modern societies.

Dr. Lillà Lionetti
Prof. Dr. Assunta Lombardi
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • bioactive compounds
  • mitochondrial bioenergetics
  • mitochondrial fusion
  • mitochondrial fission
  • ROS production
  • metaflammasome
  • metabolic diseases

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Related Special Issue

Published Papers (7 papers)

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Research

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15 pages, 1525 KiB  
Article
Anti-Inflammatory and Antioxidant Properties of Dehydrated Potato-Derived Bioactive Compounds in Intestinal Cells
by Manuela Giovanna Basilicata, Giacomo Pepe, Shara Francesca Rapa, Fabrizio Merciai, Carmine Ostacolo, Michele Manfra, Veronica Di Sarno, Giuseppina Autore, Daniela De Vita, Stefania Marzocco and Pietro Campiglia
Int. J. Mol. Sci. 2019, 20(23), 6087; https://doi.org/10.3390/ijms20236087 - 3 Dec 2019
Cited by 25 | Viewed by 4843
Abstract
Inflammation and oxidative stress are always more recognized as responsible for chronic disease at the intestinal level. Currently, a growing interest is addressed to the discovery of diet-derived products which have anti-inflammatory and antioxidant properties. This work aims to characterize the pharmacological potential [...] Read more.
Inflammation and oxidative stress are always more recognized as responsible for chronic disease at the intestinal level. Currently, a growing interest is addressed to the discovery of diet-derived products which have anti-inflammatory and antioxidant properties. This work aims to characterize the pharmacological potential of dehydrated potatoes. For this purpose, a simulated gastrointestinal digestion was carried out. The bioaccessible peptides were fractionated on the basis of their molecular weight and tested on intestinal epithelial cells (IEC-6) under oxidative and inflammatory conditions. Our results demonstrate that the tested peptide fractions were able to significantly inhibit tumor necrosis factor-α release and cycloxygenase-2 and inducible nitric oxide synthase expression. The tested peptides also showed significant antioxidant activity, being able to both reduce reactive oxygen species (ROS) release, also from mitochondria, and nitrotyrosine formation, and increase the antioxidant response by heme oxygenase-1 and superoxide dismutase expression. Moreover, the peptide fractions were able to significantly increase the wound repair in IEC-6. The obtained results indicate the anti-inflammatory and antioxidant potential of dehydrated potatoes at the intestinal level. Full article
(This article belongs to the Special Issue Targeted Protection of Bioactive Compounds to Mitochondria)
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15 pages, 2468 KiB  
Article
Adipose Tissue Mitochondrial Factors Profile after Dietary Bioactive Compound Weight Reduction Treatments in a Mice Obesity Model
by Anna Cassanye, Meritxell Martín-Gari, Manuel Portero-Otin and José CE Serrano
Int. J. Mol. Sci. 2019, 20(23), 5870; https://doi.org/10.3390/ijms20235870 - 22 Nov 2019
Cited by 2 | Viewed by 2924
Abstract
Prolonged caloric intake above energy needs disturbs the body’s ability to store and manage the excess of energy intake, leading to the onset of chronic degenerative diseases. This study aimed to compare the effect of three foods, which contain demonstrated bioactive compounds in [...] Read more.
Prolonged caloric intake above energy needs disturbs the body’s ability to store and manage the excess of energy intake, leading to the onset of chronic degenerative diseases. This study aimed to compare the effect of three foods, which contain demonstrated bioactive compounds in the treatment of obesity and as an adjuvant in obesity energy restriction treatments. In a mice obesity model induced through a high-fat diet; fish oil, soluble fibre, and soy were incorporated to evaluate its capacity to modulate metabolic factors in adipose tissue during a continued fat intake or weight reduction through a normocaloric diet. As a result, fish oil improved mitochondrial related, adipose tissue hormone expression, and oxidation products when high-fat diets are consumed; while soluble fibre improved glucose and inflammation pathways during high-fat diet intake. In weight reduction treatments few differential features, as a treatment adjuvant, were observed for fish oil and soy; while soluble fibre was able to improve the weight reduction effects induced by a normocaloric diet. As a conclusion, soluble fibre supplementation compared to an energy reduction program, was the only treatment able to induce a significant additional effect in the improvement of weight loss and adipose tissue metabolism. Full article
(This article belongs to the Special Issue Targeted Protection of Bioactive Compounds to Mitochondria)
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14 pages, 9252 KiB  
Article
High-Fish Oil and High-Lard Diets Differently Affect Testicular Antioxidant Defense and Mitochondrial Fusion/Fission Balance in Male Wistar Rats: Potential Protective Effect of ω3 Polyunsaturated Fatty Acids Targeting Mitochondria Dynamics
by Vincenzo Migliaccio, Raffaella Sica, Ilaria Di Gregorio, Rosalba Putti and Lillà Lionetti
Int. J. Mol. Sci. 2019, 20(12), 3110; https://doi.org/10.3390/ijms20123110 - 25 Jun 2019
Cited by 14 | Viewed by 5174
Abstract
High-fat diets rich in fish oil (HFO diet, mainly ω3-PUFAs), in contrast to high-fat diets rich in lard (HL diet, mainly saturated fatty acids) have been shown to induce improvement in mitochondrial function and fusion processes associated with a reduction in reactive oxygen [...] Read more.
High-fat diets rich in fish oil (HFO diet, mainly ω3-PUFAs), in contrast to high-fat diets rich in lard (HL diet, mainly saturated fatty acids) have been shown to induce improvement in mitochondrial function and fusion processes associated with a reduction in reactive oxygen species production in both liver and skeletal muscle. High-fat diets may also impair testicular function, and mitochondria represent important cellular organelles with a pivotal role in reproductive function. Mitochondria are dynamic organelles that frequently undergo fission/fusion processes. A shift toward mitochondrial fusion process has been associated with improvement of mitochondrial function, as well as with ω3-PUFAs protective effects. The present study aimed to analyze the effect of chronic overfeeding (six weeks) with HFO or HL diet on testicular tissue histology, oxidative stress, antioxidant defenses, and mitochondrial fusion (mitofusin 2) and fission (dynamic related protein 1) protein. Our results showed that HFO diet induced less testicular histology impairment, oxidative stress, and apoptosis compared to a HL diet. This finding was associated with an increase in antioxidant activities and a shift toward mitochondrial fusion processes induced by HFO diet compared to HL diet, suggesting that ω3-PUFAs may act as bioactive compound targeting mitochondria dynamics to prevent testicular impairment. Full article
(This article belongs to the Special Issue Targeted Protection of Bioactive Compounds to Mitochondria)
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16 pages, 3386 KiB  
Article
Mitochondrial Targeting of Antioxidants Alters Pancreatic Acinar Cell Bioenergetics and Determines Cell Fate
by Jane A. Armstrong, Nicole J. Cash, Jack C. Morton, Alexei V. Tepikin, Robert Sutton and David N. Criddle
Int. J. Mol. Sci. 2019, 20(7), 1700; https://doi.org/10.3390/ijms20071700 - 5 Apr 2019
Cited by 14 | Viewed by 3883
Abstract
Mitochondrial dysfunction is a core feature of acute pancreatitis, a severe disease in which oxidative stress is elevated. Mitochondrial targeting of antioxidants is a potential therapeutic strategy for this and other diseases, although thus far mixed results have been reported. We investigated the [...] Read more.
Mitochondrial dysfunction is a core feature of acute pancreatitis, a severe disease in which oxidative stress is elevated. Mitochondrial targeting of antioxidants is a potential therapeutic strategy for this and other diseases, although thus far mixed results have been reported. We investigated the effects of mitochondrial targeting with the antioxidant MitoQ on pancreatic acinar cell bioenergetics, adenosine triphosphate (ATP) production and cell fate, in comparison with the non-antioxidant control decyltriphenylphosphonium bromide (DecylTPP) and general antioxidant N-acetylcysteine (NAC). MitoQ (µM range) and NAC (mM range) caused sustained elevations of basal respiration and the inhibition of spare respiratory capacity, which was attributable to an antioxidant action since these effects were minimal with DecylTPP. Although MitoQ but not DecylTPP decreased cellular NADH levels, mitochondrial ATP turnover capacity and cellular ATP concentrations were markedly reduced by both MitoQ and DecylTPP, indicating a non-specific effect of mitochondrial targeting. All three compounds were associated with a compensatory elevation of glycolysis and concentration-dependent increases in acinar cell apoptosis and necrosis. These data suggest that reactive oxygen species (ROS) contribute a significant negative feedback control of basal cellular metabolism. Mitochondrial targeting using positively charged molecules that insert into the inner mitochondrial member appears to be deleterious in pancreatic acinar cells, as does an antioxidant strategy for the treatment of acute pancreatitis. Full article
(This article belongs to the Special Issue Targeted Protection of Bioactive Compounds to Mitochondria)
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Review

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16 pages, 1189 KiB  
Review
Natural Products Targeting ER Stress, and the Functional Link to Mitochondria
by Stefania Martucciello, Milena Masullo, Antonietta Cerulli and Sonia Piacente
Int. J. Mol. Sci. 2020, 21(6), 1905; https://doi.org/10.3390/ijms21061905 - 11 Mar 2020
Cited by 77 | Viewed by 6589
Abstract
The endoplasmic reticulum (ER) is a dynamic organelle essential for intracellular homeostasis maintenance, controlling synthesis, the folding of secreted and membrane-bound proteins, and transport of Ca2+. During cellular stress, ER dysfunction leads to the activation of unfolded protein response (UPR) due [...] Read more.
The endoplasmic reticulum (ER) is a dynamic organelle essential for intracellular homeostasis maintenance, controlling synthesis, the folding of secreted and membrane-bound proteins, and transport of Ca2+. During cellular stress, ER dysfunction leads to the activation of unfolded protein response (UPR) due to accumulated misfolded proteins in the ER. This condition is referred as ER stress. Mitochondria and ER form a site of close contact (the mitochondria-associated membrane, MAM) which is a major platform exerting important physiological roles in the regulation of intracellular Ca2+ homeostasis, lipid metabolism, mitochondrial fission, autophagosome formation, and apoptosis progression. Natural products have been receiving increasing attention for their ability to interfere with ER stress. Research works have focused on the capacity of these bioactive compounds to induce apoptosis by activating ER stress through the ER stress-mediated mitochondrial apoptotic pathway. In this review we discuss the role of natural products in the signaling communication between ER and mitochondria, focusing on the effects induced by ER stress including Ca2+ permeability transition and UPR signaling (protein kinase R-like ER kinase/mitofusin 2). Full article
(This article belongs to the Special Issue Targeted Protection of Bioactive Compounds to Mitochondria)
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13 pages, 1539 KiB  
Review
Impact of Glucoraphanin-Mediated Activation of Nrf2 on Non-Alcoholic Fatty Liver Disease with a Focus on Mitochondrial Dysfunction
by Liang Xu, Naoto Nagata and Tsuguhito Ota
Int. J. Mol. Sci. 2019, 20(23), 5920; https://doi.org/10.3390/ijms20235920 - 25 Nov 2019
Cited by 41 | Viewed by 8296
Abstract
Non-alcoholic fatty liver disease (NAFLD) is a common disease in Western nations and ranges in severity from steatosis to steatohepatitis (NASH). NAFLD is a genetic-environmental-metabolic stress-related disease of unclear pathogenesis. NAFLD is triggered by caloric overconsumption and physical inactivity, which lead to insulin [...] Read more.
Non-alcoholic fatty liver disease (NAFLD) is a common disease in Western nations and ranges in severity from steatosis to steatohepatitis (NASH). NAFLD is a genetic-environmental-metabolic stress-related disease of unclear pathogenesis. NAFLD is triggered by caloric overconsumption and physical inactivity, which lead to insulin resistance and oxidative stress. A growing body of evidence indicates that mitochondrial dysfunction plays a critical role in the pathogenesis of NAFLD. Mitochondrial dysfunction not only promotes fat accumulation, but also leads to generation of reactive oxygen species (ROS) and lipid peroxidation, resulting in oxidative stress in hepatocytes. Nuclear factor erythroid 2-related factor 2 (Nrf2) is an important modulator of antioxidant signaling that serves as a primary cellular defense against the cytotoxic effects of oxidative stress. The pharmacological induction of Nrf2 ameliorates obesity-associated insulin resistance and NAFLD in a mouse model. Sulforaphane and its precursor glucoraphanin are derived from broccoli sprouts and are the most potent natural Nrf2 inducers—they may protect mitochondrial function, thus suppressing the development of NASH. In this review, we briefly describe the role of mitochondrial dysfunction in the pathogenesis of NASH and the effects of glucoraphanin on its development. Full article
(This article belongs to the Special Issue Targeted Protection of Bioactive Compounds to Mitochondria)
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31 pages, 2576 KiB  
Review
Mitochondria in Neuroprotection by Phytochemicals: Bioactive Polyphenols Modulate Mitochondrial Apoptosis System, Function and Structure
by Makoto Naoi, Yuqiu Wu, Masayo Shamoto-Nagai and Wakako Maruyama
Int. J. Mol. Sci. 2019, 20(10), 2451; https://doi.org/10.3390/ijms20102451 - 17 May 2019
Cited by 118 | Viewed by 11450
Abstract
In aging and neurodegenerative diseases, loss of distinct type of neurons characterizes disease-specific pathological and clinical features, and mitochondria play a pivotal role in neuronal survival and death. Mitochondria are now considered as the organelle to modulate cellular signal pathways and functions, not [...] Read more.
In aging and neurodegenerative diseases, loss of distinct type of neurons characterizes disease-specific pathological and clinical features, and mitochondria play a pivotal role in neuronal survival and death. Mitochondria are now considered as the organelle to modulate cellular signal pathways and functions, not only to produce energy and reactive oxygen species. Oxidative stress, deficit of neurotrophic factors, and multiple other factors impair mitochondrial function and induce cell death. Multi-functional plant polyphenols, major groups of phytochemicals, are proposed as one of most promising mitochondria-targeting medicine to preserve the activity and structure of mitochondria and neurons. Polyphenols can scavenge reactive oxygen and nitrogen species and activate redox-responsible transcription factors to regulate expression of genes, coding antioxidants, anti-apoptotic Bcl-2 protein family, and pro-survival neurotrophic factors. In mitochondria, polyphenols can directly regulate the mitochondrial apoptosis system either in preventing or promoting way. Polyphenols also modulate mitochondrial biogenesis, dynamics (fission and fusion), and autophagic degradation to keep the quality and number. This review presents the role of polyphenols in regulation of mitochondrial redox state, death signal system, and homeostasis. The dualistic redox properties of polyphenols are associated with controversial regulation of mitochondrial apoptosis system involved in the neuroprotective and anti-carcinogenic functions. Mitochondria-targeted phytochemical derivatives were synthesized based on the phenolic structure to develop a novel series of neuroprotective and anticancer compounds, which promote the bioavailability and effectiveness. Phytochemicals have shown the multiple beneficial effects in mitochondria, but further investigation is required for the clinical application. Full article
(This article belongs to the Special Issue Targeted Protection of Bioactive Compounds to Mitochondria)
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