ijms-logo

Journal Browser

Journal Browser

Interventions Affecting the Mitochondrial Control of Longevity and Health

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 (30 April 2021) | Viewed by 10962

Special Issue Editors


E-Mail Website
Guest Editor
Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari, 70125 Bari, Italy
Interests: aging; mitochondrial biogenesis in aging; mitochondrial pathologies; pathologies with mitochondrial oxidative stress (age-related diseases, autoimmune and inflammatory pathologies, neurodegenerative diseases); calorie restriction and nutritional anti-aging interventions; mtDNA–TFAM relationships
Special Issues, Collections and Topics in MDPI journals
Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari, 70125 Bari, Italy
Interests: mtDNA damage and deletions; mitochondrial oxidative stress and antioxidant defense; mitochondrial biogenesis and dynamics; mitochondrial quality control; mitochondrial dysfunction in aging and age-related degenerative disorders; nutritional anti-aging interventions
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari, 70125 Bari, Italy
Interests: interplay between inflammation and oxidative stress; nutritional interventions; qualitative and quantitative alterations of mtDNA; mitochondrial biogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Research on mitochondria has progressively unveiled that these organelles are not only the major source of cell ATP, but they are also involved in several crucial processes as regulation of the overall redox state through reactive oxygen species (ROS), apoptosis, Ca2+ storage and handling, waste disposal and metabolites biosynthesis. Mitochondria partake also in signaling pathways that, through sensing alterations in genome damage level or in nutrients and energy availability, regulate cell metabolism. Such metabolic tuning up can be pursued also by means of the fine regulation of mitochondrial homeostasis obtained by balancing biogenesis, dynamics, and mitophagy. The disclosure of the multiple roles performed by mitochondria has proceeded in parallel with the discovery of the complex interplay connecting such functions and of its relevance in modulating health conditions and the aging process of the whole organism. Furthermore, the mitochondrial interplay has been shown to be highly dynamic and sensitive to different external stimuli as nutritional regimens, lifestyle habits, and medicine administrations are able to affect cell homeostasis and energy production. The dissection of the molecular mechanisms underlying such a wide range of genetic, nutritional, pharmacological, and lifestyle interventions has proceeded at a fast pace also because of their potentiality to extend longevity as well as to promote human health. The possibility to understand and to influence, at the molecular level, the multifaceted mitochondrial responses has inspired the utilization of multiple experimental systems and approaches, leading to a constantly growing, huge amount of data.

This Special Issue about “Interventions affecting the mitochondrial control of longevity and health” aims to provide, from a molecular standpoint, a broad and updated overview of present models and future strategies that might assist in deepening the knowledge of such an intricate issue. Contributions by experts of the field in the form of research papers and critical reviews are called for.

Prof. Dr. Angela Maria Serena Lezza
Prof. Dr. Vito Pesce
Prof. Dr. Guglielmina Chimienti
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.

Published Papers (3 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

13 pages, 4140 KiB  
Article
The Ketogenic Diet Reduces the Harmful Effects of Stress on Gut Mitochondrial Biogenesis in a Rat Model of Irritable Bowel Syndrome
by Guglielmina Chimienti, Antonella Orlando, Angela Maria Serena Lezza, Benedetta D’Attoma, Maria Notarnicola, Isabella Gigante, Vito Pesce and Francesco Russo
Int. J. Mol. Sci. 2021, 22(7), 3498; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22073498 - 28 Mar 2021
Cited by 12 | Viewed by 3729
Abstract
Functional alterations in irritable bowel syndrome have been associated with defects in bioenergetics and the mitochondrial network. Effects of high fat, adequate-protein, low carbohydrate ketogenic diet (KD) involve oxidative stress, inflammation, mitochondrial function, and biogenesis. The aim was to evaluate the KD efficacy [...] Read more.
Functional alterations in irritable bowel syndrome have been associated with defects in bioenergetics and the mitochondrial network. Effects of high fat, adequate-protein, low carbohydrate ketogenic diet (KD) involve oxidative stress, inflammation, mitochondrial function, and biogenesis. The aim was to evaluate the KD efficacy in reducing the effects of stress on gut mitochondria. Newborn Wistar rats were exposed to maternal deprivation to induce IBS in adulthood. Intestinal inflammation (COX-2 and TRL-4); cellular redox status (SOD 1, SOD 2, PrxIII, mtDNA oxidatively modified purines); mitochondrial biogenesis (PPAR-γ, PGC-1α, COX-4, mtDNA content); and autophagy (Beclin-1, LC3 II) were evaluated in the colon of exposed rats fed with KD (IBD-KD) or standard diet (IBS-Std), and in unexposed controls (Ctrl). IBS-Std rats showed dysfunctional mitochondrial biogenesis (PPAR-γ, PGC-1α, COX-4, and mtDNA contents lower than in Ctrl) associated with inflammation and increased oxidative stress (higher levels of COX-2 and TLR-4, SOD 1, SOD 2, PrxIII, and oxidatively modified purines than in Ctrl). Loss of autophagy efficacy appeared from reduced levels of Beclin-1 and LC3 II. Feeding of animals with KD elicited compensatory mechanisms able to reduce inflammation, oxidative stress, restore mitochondrial function, and baseline autophagy, possibly via the upregulation of the PPAR-γ/PGC-1α axis. Full article
Show Figures

Figure 1

18 pages, 2542 KiB  
Article
The Age-Sensitive Efficacy of Calorie Restriction on Mitochondrial Biogenesis and mtDNA Damage in Rat Liver
by Guglielmina Chimienti, Anna Picca, Flavio Fracasso, Francesco Russo, Antonella Orlando, Giuseppe Riezzo, Christiaan Leeuwenburgh, Vito Pesce and Angela Maria Serena Lezza
Int. J. Mol. Sci. 2021, 22(4), 1665; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22041665 - 07 Feb 2021
Cited by 15 | Viewed by 2584
Abstract
Calorie restriction (CR) is the most efficacious treatment to delay the onset of age-related changes such as mitochondrial dysfunction. However, the sensitivity of mitochondrial markers to CR and the age-related boundaries of CR efficacy are not fully elucidated. We used liver samples from [...] Read more.
Calorie restriction (CR) is the most efficacious treatment to delay the onset of age-related changes such as mitochondrial dysfunction. However, the sensitivity of mitochondrial markers to CR and the age-related boundaries of CR efficacy are not fully elucidated. We used liver samples from ad libitum-fed (AL) rats divided in: 18-month-old (AL-18), 28-month-old (AL-28), and 32-month-old (AL-32) groups, and from CR-treated (CR) 28-month-old (CR-28) and 32-month-old (CR-32) counterparts to assay the effect of CR on several mitochondrial markers. The age-related decreases in citrate synthase activity, in TFAM, MFN2, and DRP1 protein amounts and in the mtDNA content in the AL-28 group were prevented in CR-28 counterparts. Accordingly, CR reduced oxidative mtDNA damage assessed through the incidence of oxidized purines at specific mtDNA regions in CR-28 animals. These findings support the anti-aging effect of CR up to 28 months. Conversely, the protein amounts of LonP1, Cyt c, OGG1, and APE1 and the 4.8 Kb mtDNA deletion content were not affected in CR-28 rats. The absence of significant differences between the AL-32 values and the CR-32 counterparts suggests an age-related boundary of CR efficacy at this age. However, this only partially curtails the CR benefits in counteracting the generalized aging decline and the related mitochondrial involvement. Full article
Show Figures

Figure 1

19 pages, 3150 KiB  
Article
Aberrant Mitochondrial Morphology and Function in the BTBR Mouse Model of Autism Is Improved by Two Weeks of Ketogenic Diet
by Younghee Ahn, Rasha Sabouny, Bianca R. Villa, Nellie C. Yee, Richelle Mychasiuk, Golam M. Uddin, Jong M. Rho and Timothy E. Shutt
Int. J. Mol. Sci. 2020, 21(9), 3266; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21093266 - 05 May 2020
Cited by 32 | Viewed by 4144
Abstract
Autism spectrum disorder (ASD) is a highly prevalent neurodevelopmental disorder that exhibits a common set of behavioral and cognitive impairments. Although the etiology of ASD remains unclear, mitochondrial dysfunction has recently emerged as a possible causative factor underlying ASD. The ketogenic diet (KD) [...] Read more.
Autism spectrum disorder (ASD) is a highly prevalent neurodevelopmental disorder that exhibits a common set of behavioral and cognitive impairments. Although the etiology of ASD remains unclear, mitochondrial dysfunction has recently emerged as a possible causative factor underlying ASD. The ketogenic diet (KD) is a high-fat, low-carbohydrate diet that augments mitochondrial function, and has been shown to reduce autistic behaviors in both humans and in rodent models of ASD. The aim of the current study was to examine mitochondrial bioenergetics in the BTBR mouse model of ASD and to determine whether the KD improves mitochondrial function. We also investigated changes in mitochondrial morphology, which can directly influence mitochondrial function. We found that BTBR mice had altered mitochondrial function and exhibited smaller more fragmented mitochondria compared to C57BL/6J controls, and that supplementation with the KD improved both mitochondrial function and morphology. We also identified activating phosphorylation of two fission proteins, pDRP1S616 and pMFFS146, in BTBR mice, consistent with the increased mitochondrial fragmentation that we observed. Intriguingly, we found that the KD decreased pDRP1S616 levels in BTBR mice, likely contributing to the restoration of mitochondrial morphology. Overall, these data suggest that impaired mitochondrial bioenergetics and mitochondrial fragmentation may contribute to the etiology of ASD and that these alterations can be reversed with KD treatment. Full article
Show Figures

Figure 1

Back to TopTop