Submit to Special Issue Submit Abstract to Special Issue Review for IJMS Propose a Special Issue

Journal Menu

Journal Browser

Research on Mitochondria and Cell Death in Disease Diagnosis and Treatment

Print Special Issue Flyer
Special Issue Editors
Special Issue Information
Keywords
Benefits of Publishing in a Special Issue
Published Papers
Planned Papers

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: 25 March 2025 | Viewed by 27953

Share This Special Issue

Special Issue Editor

Dr. Venediktova Natalya

E-Mail Website
Guest Editor

Institute of Theoretical and Experimental Biophysics Russian Academy of Sciences, Pushchino, Moscow Region 142290, Russia
Interests: mitochondrial dysfunction; reactive oxygen species; oxidative stress; lipid peroxidation; mitochondrial dynamics; mitophagy; mitochondrial biogenesis; apoptosis; neurodegeneration; metabolic syndrome; mitochondria-targeted antioxidants; diseases associated with mitochondrial dysfunction, diagnosis and treatment

Special Issue Information

Dear Colleagues,

Mitochondria are essential organelles for many aspects of cellular homeostasis, including energy production by oxidative phosphorylation. Mitochondrial metabolism links energy production with other important cellular processes, such as signal transduction, cell differentiation, and apoptosis. In addition to producing adenosine triphosphate (ATP) as an energy source, mitochondria are responsible for the synthesis of many important metabolites and cofactors, such as tetrahydrofolate, α-keto acids, steroids, aminolevulinic acid, biotin, lipoic acid, acetyl-CoA, iron–sulfur clusters, heme and ubiquinone. In addition, mitochondria and their metabolism are involved in aging and a number of human diseases. Diseases defined by mitochondrial dysfunction have expanded from rare monogenic disorders to metabolic, cardiovascular, neurodegenerative and neuromuscular diseases. Therefore, there is great interest in understanding mitochondrial metabolism and the complex relationship it possesses with other cellular processes. This has led to an intensive search for new therapeutic and prophylactic strategies aimed at activating mitochondrial function by using key components of mitochondrial biogenesis, redox metabolism, dynamics and mitophagy.

This Special Issue will discuss the complexity of the molecular mechanisms that regulate mitochondria at multiple levels, as well as their role in the pathophysiology of diseases and the development of new therapeutic strategies. Topics of interest include, but are not limited to, the following: diagnosis and treatment of mitochondrial dysfunctions, reactive oxygen specifications, oxidative stress, lipid peroxidation, mitochondrial dynamics, mitophagy, mitochondrial biogenesis, apoptosis and diseases related to mitochondrial dysfunction.

Dr. Venediktova Natalya
Guest Editor

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

mitochondrial dysfunction
reactive oxygen species
oxidative stress
lipid peroxidation
mitochondrial dynamics
mitophagy
mitochondrial biogenesis
apoptosis
neurodegeneration
metabolic syndrome
mitochondria-targeted antioxidants
diseases associated with mitochondrial dysfunction, diagnosis and treatment

Benefits of Publishing in a Special Issue

Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (12 papers)

Download All Papers

Order results

Result details

Show export options Show export options

Select all

Export citation of selected articles as:

Research

Jump to: Review

16 pages, 4533 KiB

Open AccessArticle

Mitochondrial Dysfunction Causes Cell Death in Patients Affected by Fragile-X-Associated Disorders

by Martina Grandi, Chiara Galber, Cristina Gatto, Veronica Nobile, Cecilia Pucci, Ida Schaldemose Nielsen, Francesco Boldrin, Giovanni Neri, Pietro Chiurazzi, Giancarlo Solaini, Alessandra Baracca, Valentina Giorgio and Elisabetta Tabolacci

Int. J. Mol. Sci. 2024, 25(6), 3421; https://doi.org/10.3390/ijms25063421 - 18 Mar 2024

Cited by 1 | Viewed by 1595

Abstract

Mitochondria are involved in multiple aspects of neurodevelopmental processes and play a major role in the pathogenetic mechanisms leading to neuro-degenerative diseases. Fragile-X-related disorders (FXDs) are genetic conditions that occur due to the dynamic expansion of CGG repeats of the FMR1 gene encoding for the RNA-binding protein FMRP, particularly expressed in the brain. This gene expansion can lead to premutation (PM, 56–200 CGGs), full mutation (FM, >200 CGGs), or unmethylated FM (UFM), resulting in neurodegeneration, neurodevelopmental disorders, or no apparent intellectual disability, respectively. To investigate the mitochondrial mechanisms that are involved in the FXD patients, we analyzed mitochondrial morphology and bioenergetics in fibroblasts derived from patients. Donut-shaped mitochondrial morphology and excessive synthesis of critical mitochondrial proteins were detected in FM, PM, and UFM cells. Analysis of mitochondrial oxidative phosphorylation in situ reveals lower respiration in PM fibroblasts. Importantly, mitochondrial permeability transition-dependent apoptosis is sensitized to reactive oxygen species in FM, PM, and UFM models. This study elucidated the mitochondrial mechanisms that are involved in the FXD phenotypes, and indicated altered mitochondrial function and morphology. Importantly, a sensitization to permeability transition and apoptosis was revealed in FXD cells. Overall, our data suggest that mitochondria are novel drug targets to relieve the FXD symptoms. Full article

(This article belongs to the Special Issue Research on Mitochondria and Cell Death in Disease Diagnosis and Treatment)

► Show Figures

Figure 1

17 pages, 4584 KiB

Open AccessArticle

Downregulation of Mitochondrial Fusion Protein Expression Affords Protection from Canonical Necroptosis in H9c2 Cardiomyoblasts

by Yuki Toda, Sang-Bing Ong, Toshiyuki Yano, Atsushi Kuno, Hidemichi Kouzu, Tatsuya Sato, Wataru Ohwada, Yuki Tatekoshi, Toshifumi Ogawa, Masaki Shimizu, Masaya Tanno and Masato Furuhashi

Int. J. Mol. Sci. 2024, 25(5), 2905; https://doi.org/10.3390/ijms25052905 - 2 Mar 2024

Cited by 2 | Viewed by 1510

Abstract

Necroptosis, a form of necrosis, and alterations in mitochondrial dynamics, a coordinated process of mitochondrial fission and fusion, have been implicated in the pathogenesis of cardiovascular diseases. This study aimed to determine the role of mitochondrial morphology in canonical necroptosis induced by a combination of TNFα and zVAD (TNF/zVAD) in H9c2 cells, rat cardiomyoblasts. Time-course analyses of mitochondrial morphology showed that mitochondria were initially shortened after the addition of TNF/zVAD and then their length was restored, and the proportion of cells with elongated mitochondria at 12 h was larger in TNF/zVAD-treated cells than in non-treated cells (16.3 ± 0.9% vs. 8.0 ± 1.2%). The knockdown of dynamin-related protein 1 (Drp1) and fission 1, fission promoters, and treatment with Mdivi-1, a Drp-1 inhibitor, had no effect on TNF/zVAD-induced necroptosis. In contrast, TNF/zVAD-induced necroptosis was attenuated by the knockdown of mitofusin 1/2 (Mfn1/2) and optic atrophy-1 (Opa1), proteins that are indispensable for mitochondrial fusion, and the attenuation of necroptosis was not canceled by treatment with Mdivi-1. The expression of TGFβ-activated kinase (TAK1), a negative regulator of RIP1 activity, was upregulated and the TNF/zVAD-induced RIP1-Ser166 phosphorylation, an index of RIP1 activity, was mitigated by the knockdown of Mfn1/2 or Opa1. Pharmacological TAK1 inhibition attenuated the protection afforded by Mfn1/2 and Opa1 knockdown. In conclusion, the inhibition of mitochondrial fusion increases TAK1 expression, leading to the attenuation of canonical necroptosis through the suppression of RIP1 activity. Full article

(This article belongs to the Special Issue Research on Mitochondria and Cell Death in Disease Diagnosis and Treatment)

► Show Figures

Figure 1

17 pages, 2400 KiB

Open AccessArticle

GDF15 Protects Insulin-Producing Beta Cells against Pro-Inflammatory Cytokines and Metabolic Stress via Increased Deamination of Intracellular Adenosine

by Anongnad Ngamjariyawat, Jing Cen, Xuan Wang and Nils Welsh

Int. J. Mol. Sci. 2024, 25(2), 801; https://doi.org/10.3390/ijms25020801 - 8 Jan 2024

Cited by 4 | Viewed by 1964

Abstract

It has been proposed that antidiabetic drugs, such as metformin and imatinib, at least in part, promote improved glucose tolerance in type 2 diabetic patients via increased production of the inflammatory cytokine GDF15. This is supported by studies, performed in rodent cell lines and mouse models, in which the addition or production of GDF15 improved beta-cell function and survival. The aim of the present study was to determine whether human beta cells produce GDF15 in response to antidiabetic drugs and, if so, to further elucidate the mechanisms by which GDF15 modulates the function and survival of such cells. The effects and expression of GDF15 were analyzed in human insulin-producing EndoC-betaH1 cells and human islets. We observed that alpha and beta cells exhibit considerable heterogeneity in GDF15 immuno-positivity. The predominant form of GDF15 present in islet and EndoC-betaH1 cells was pro-GDF15. Imatinib, but not metformin, increased pro-GDF15 levels in EndoC-betaH1 cells. Under basal conditions, exogenous GDF15 increased human islet oxygen consumption rates. In EndoC-betaH1 cells and human islets, exogenous GDF15 partially ameliorated cytokine- or palmitate + high-glucose-induced loss of function and viability. GDF15-induced cell survival was paralleled by increased inosine levels, suggesting a more efficient disposal of intracellular adenosine. Knockdown of adenosine deaminase, the enzyme that converts adenosine to inosine, resulted in lowered inosine levels and loss of protection against cytokine- or palmitate + high-glucose-induced cell death. It is concluded that imatinib-induced GDF15 production may protect human beta cells partially against inflammatory and metabolic stress. Furthermore, it is possible that the GDF15-mediated activation of adenosine deaminase and the increased disposal of intracellular adenosine participate in protection against beta-cell death. Full article

(This article belongs to the Special Issue Research on Mitochondria and Cell Death in Disease Diagnosis and Treatment)

► Show Figures

Graphical abstract

16 pages, 5051 KiB

Open AccessArticle

Investigating the Mitoprotective Effects of S1P Receptor Modulators Ex Vivo Using a Novel Semi-Automated Live Imaging Set-Up

by Rebecca Ludwig, Bimala Malla, Maria Höhrhan, Carmen Infante-Duarte and Lina Anderhalten

Int. J. Mol. Sci. 2024, 25(1), 261; https://doi.org/10.3390/ijms25010261 - 23 Dec 2023

Viewed by 1276

Abstract

In multiple sclerosis (MS), mitochondrial alterations appear to contribute to disease progression. The sphingosine-1-phosphate receptor modulator siponimod is approved for treating secondary progressive MS. Its preceding compound fingolimod was shown to prevent oxidative stress-induced alterations in mitochondrial morphology. Here, we assessed the effects of siponimod, compared to fingolimod, on neuronal mitochondria in oxidatively stressed hippocampal slices. We have also advanced the model of chronic organotypic hippocampal slices for live imaging, enabling semi-automated monitoring of mitochondrial alterations. The slices were prepared from B6.Cg-Tg(Thy1-CFP/COX8A)S2Lich/J mice that display fluorescent neuronal mitochondria. They were treated with hydrogen peroxide (oxidative stress paradigm) ± 1 nM siponimod or fingolimod for 24 h. Afterwards, mitochondrial dynamics were investigated. Under oxidative stress, the fraction of motile mitochondria decreased and mitochondria were shorter, smaller, and covered smaller distances. Siponimod partly prevented oxidatively induced alterations in mitochondrial morphology; for fingolimod, a similar trend was observed. Siponimod reduced the decrease in mitochondrial track displacement, while both compounds significantly increased track speed and preserved motility. The novel established imaging and analysis tools are suitable for assessing the dynamics of neuronal mitochondria ex vivo. Using these approaches, we showed that siponimod at 1 nM partially prevented oxidatively induced mitochondrial alterations in chronic brain slices. Full article

(This article belongs to the Special Issue Research on Mitochondria and Cell Death in Disease Diagnosis and Treatment)

► Show Figures

Figure 1

19 pages, 3695 KiB

Open AccessArticle

Novel Relationship between Mitofusin 2-Mediated Mitochondrial Hyperfusion, Metabolic Remodeling, and Glycolysis in Pulmonary Arterial Endothelial Cells

by Manivannan Yegambaram, Xutong Sun, Alejandro Garcia Flores, Qing Lu, Jamie Soto, Jaime Richards, Saurabh Aggarwal, Ting Wang, Haiwei Gu, Jeffrey R. Fineman and Stephen M. Black

Int. J. Mol. Sci. 2023, 24(24), 17533; https://doi.org/10.3390/ijms242417533 - 15 Dec 2023

Cited by 4 | Viewed by 1849

Abstract

The disruption of mitochondrial dynamics has been identified in cardiovascular diseases, including pulmonary hypertension (PH), ischemia-reperfusion injury, heart failure, and cardiomyopathy. Mitofusin 2 (Mfn2) is abundantly expressed in heart and pulmonary vasculature cells at the outer mitochondrial membrane to modulate fusion. Previously, we have reported reduced levels of Mfn2 and fragmented mitochondria in pulmonary arterial endothelial cells (PAECs) isolated from a sheep model of PH induced by pulmonary over-circulation and restoring Mfn2 normalized mitochondrial function. In this study, we assessed the effect of increased expression of Mfn2 on mitochondrial metabolism, bioenergetics, reactive oxygen species production, and mitochondrial membrane potential in control PAECs. Using an adenoviral expression system to overexpress Mfn2 in PAECs and utilizing ¹³C labeled substrates, we assessed the levels of TCA cycle metabolites. We identified increased pyruvate and lactate production in cells, revealing a glycolytic phenotype (Warburg phenotype). Mfn2 overexpression decreased the mitochondrial ATP production rate, increased the rate of glycolytic ATP production, and disrupted mitochondrial bioenergetics. The increase in glycolysis was linked to increased hypoxia-inducible factor 1α (HIF-1α) protein levels, elevated mitochondrial reactive oxygen species (mt-ROS), and decreased mitochondrial membrane potential. Our data suggest that disrupting the mitochondrial fusion/fission balance to favor hyperfusion leads to a metabolic shift that promotes aerobic glycolysis. Thus, therapies designed to increase mitochondrial fusion should be approached with caution. Full article

(This article belongs to the Special Issue Research on Mitochondria and Cell Death in Disease Diagnosis and Treatment)

► Show Figures

Figure 1

15 pages, 3968 KiB

Open AccessArticle

Lovastatin Treatment Inducing Apoptosis in Human Pancreatic Cancer Cells by Inhibiting Cholesterol Rafts in Plasma Membrane and Mitochondria

by Momoko Gyoten, Yi Luo, Rina Fujiwara-Tani, Shiori Mori, Ruiko Ogata, Shingo Kishi and Hiroki Kuniyasu

Int. J. Mol. Sci. 2023, 24(23), 16814; https://doi.org/10.3390/ijms242316814 - 27 Nov 2023

Cited by 2 | Viewed by 1902

Abstract

Resistance to anticancer drugs is a problem in the treatment of pancreatic ductal carcinoma (PDAC) and overcoming it is an important issue. Recently, it has been reported that statins induce apoptosis in cancer cells but the mechanism has not been completely elucidated. We investigated the antitumor mechanisms of statins against PDAC and their impact on resistance to gemcitabine (GEM). Lovastatin (LOVA) increased mitochondrial oxidative stress in PDAC cells, leading to apoptosis. LOVA reduced lipid rafts in the plasma membrane and mitochondria, suppressed the activation of epithelial growth factor receptor (EGFR) and AKT in plasma membrane rafts, and reduced B-cell lymphoma 2 (BCL2)-Bcl-2-associated X protein (BAX) binding and the translocation of F1F0 ATPase in mitochondrial rafts. In the three GEM-resistant cell lines derived from MIA and PANC1, the lipid rafts in the cell membrane and the mitochondria were increased to activate EGFR and AKT and to increase BCL2-BAX binding, which suppressed apoptosis. LOVA abrogated these anti-apoptotic effects by reducing the rafts in the resistant cells. By treating the resistant cells with LOVA, GEM sensitivity improved to the level of the parental cells. Therefore, cholesterol rafts contribute to drug resistance in PDAC. Further clinical research is warranted on overcoming anticancer drug resistance by statin-mediated intracellular cholesterol regulation. Full article

(This article belongs to the Special Issue Research on Mitochondria and Cell Death in Disease Diagnosis and Treatment)

► Show Figures

Figure 1

13 pages, 1474 KiB

Open AccessArticle

Effects of the Long-Term Administration of Uridine on the Functioning of Rat Liver Mitochondria in Hyperthyroidism

by Natalya Venediktova, Ilya Solomadin, Anna Nikiforova, Konstantin N. Belosludtsev and Galina Mironova

Int. J. Mol. Sci. 2023, 24(23), 16730; https://doi.org/10.3390/ijms242316730 - 24 Nov 2023

Viewed by 1503

Abstract

The effect of uridine (30 mg/kg for 7 days; intraperitoneally) on the functions of liver mitochondria in rats with experimentally induced hyperthyroidism (HT) (200 µg/100 g for 7 days, intraperitoneally) is studied in this paper. An excess of thyroid hormones (THs) led to an intensification of energy metabolism, the development of oxidative stress, a significant increase in the biogenesis, and changes in the content of proteins responsible for the fusion and fission of mitochondria. The injection of uridine did not change the concentration of THs in the blood of hyperthyroid rats (HRs) but normalized their body weight. The exposure to uridine improved the parameters of oxidative phosphorylation and corrected the activity of some complexes of the electron transport chain (ETC) in the liver mitochondria of HRs. The analysis of ETC complexes showed that the level of CI–CV did not change by the action of uridine in rats with the condition of HT. The application of uridine caused a significant increase in the activity of superoxide dismutase and lowered the rate of hydrogen peroxide production. It was found that uridine affected mitochondrial biogenesis by increasing the expression of the genes Ppargc1a and NRF1 and diminishing the expression of the Parkin gene responsible for mitophagy compared with the control animals. In addition, the mRNA level of the OPA1 gene was restored, which may indicate an improvement in the ETC activity and oxidative phosphorylation in the mitochondria of HR. As a whole, the results obtained demonstrate that uridine has a protective effect against HT-mediated functional disorders in the metabolism of rat liver mitochondria. Full article

(This article belongs to the Special Issue Research on Mitochondria and Cell Death in Disease Diagnosis and Treatment)

► Show Figures

Figure 1

19 pages, 5240 KiB

Open AccessArticle

Direct-Acting Antiviral Drug Modulates the Mitochondrial Biogenesis in Different Tissues of Young Female Rats

by Hala A. Hafez, Ali M. Atoom, Rana H. M. Khafaga, Sara A. Shaker, Maher A. Kamel, Nagwa M. Assem and Shimaa A. Mahmoud

Int. J. Mol. Sci. 2023, 24(21), 15844; https://doi.org/10.3390/ijms242115844 - 31 Oct 2023

Viewed by 1214

Abstract

(1) Background: Hepatitis C virus (HCV) infection is endemic in Egypt, with the highest prevalence rate worldwide. Sofosbuvir (SOF) is a nucleos(t)ide analog that specifically inhibits HCV replication. This study aimed to explore the possible effects of the therapeutic dose of SOF on the mitochondrial biogenesis and functions of the liver, muscle, and ovarian tissues of young normal female rats. (2) Methods: This study was conducted on 20 female Wistar rats, classified into two groups, the control group and the exposed group; the latter was orally supplemented with 4 mg/kg/day of SOF for 3 months. (3) Results: The exposure to SOF impairs mitochondrial biogenesis via mitochondrial DNA copy number decline and suppressed mitochondrial biogenesis-regulated parameters at mRNA and protein levels. Also, SOF suppresses the DNA polymerase γ (POLG) expression, citrate synthase activity, and mitochondrial NADH dehydrogenase subunit-5 (ND5) content, which impairs mitochondrial functions. SOF increased lipid peroxidation and oxidative DNA damage markers and decreased tissue expression of nuclear factor erythroid 2-related factor 2 (Nfe2l2). (4) Conclusions: The present findings demonstrate the adverse effects of SOF on mitochondrial biogenesis and function in different tissues of young female rats, which mostly appeared in ovarian tissues. Full article

(This article belongs to the Special Issue Research on Mitochondria and Cell Death in Disease Diagnosis and Treatment)

► Show Figures

Figure 1

12 pages, 2271 KiB

Open AccessArticle

Effects of Mitochondrial Transplantation on Transcriptomics in a Polymicrobial Sepsis Model

by Seongmin Kim, Ji Heon Noh, Min Ji Lee, Ye Jin Park, Bo Mi Kim, Yun-Seok Kim, Sangik Hwang, Chungoo Park and Kyuseok Kim

Int. J. Mol. Sci. 2023, 24(20), 15326; https://doi.org/10.3390/ijms242015326 - 18 Oct 2023

Viewed by 1504

Abstract

Previously, we demonstrated that mitochondrial transplantation has beneficial effects in a polymicrobial sepsis model. However, the mechanism has not been fully investigated. Mitochondria have their own genes, and genomic changes in sepsis are an important issue in terms of pathophysiology, biomarkers, and therapeutic targets. To investigate the changes in transcriptomic features after mitochondrial transplantation in a polymicrobial sepsis model, we used a rat model of fecal slurry polymicrobial sepsis. Total RNA from splenocytes of sham-operated (SHAM, n = 10), sepsis-induced (SEPSIS, n = 7), and sepsis receiving mitochondrial transplantation (SEPSIS + MT, n = 8) samples was extracted and we conducted a comparative transcriptome-wide analysis between three groups. We also confirmed these results with qPCR. In terms of percentage of mitochondrial mapped reads, the SEPSIS + MT group had a significantly higher mapping ratio than the others. RT1-M2 and Cbln2 were identified as highly expressed in SEPSIS + MT compared with SEPSIS. Using SHAM expression levels as another control variable, we further identified six genes (Fxyd4, Apex2l1, Kctd4, 7SK, SNORD94, and SNORA53) that were highly expressed after sepsis induction and observed that their expression levels were attenuated by mitochondrial transplantation. Changes in transcriptomic features were identified after mitochondrial transplantation in sepsis. This might provide a hint for exploring the mechanism of mitochondrial transplantation in sepsis. Full article

(This article belongs to the Special Issue Research on Mitochondria and Cell Death in Disease Diagnosis and Treatment)

► Show Figures

Figure 1

Review

Jump to: Research

16 pages, 1417 KiB

Open AccessReview

The Key Role of Mitochondria in Somatic Stem Cell Differentiation: From Mitochondrial Asymmetric Apportioning to Cell Fate

by Ilario Amato, Sébastien Meurant and Patricia Renard

Int. J. Mol. Sci. 2023, 24(15), 12181; https://doi.org/10.3390/ijms241512181 - 29 Jul 2023

Cited by 4 | Viewed by 3128

Abstract

The study of the mechanisms underlying stem cell differentiation is under intensive research and includes the contribution of a metabolic switch from glycolytic to oxidative metabolism. While mitochondrial biogenesis has been previously demonstrated in number of differentiation models, it is only recently that the role of mitochondrial dynamics has started to be explored. The discovery of asymmetric distribution of mitochondria in stem cell progeny has strengthened the interest in the field. This review attempts to summarize the regulation of mitochondrial asymmetric apportioning by the mitochondrial fusion, fission, and mitophagy processes as well as emphasize how asymmetric mitochondrial apportioning in stem cells affects their metabolism, and thus epigenetics, and determines cell fate. Full article

(This article belongs to the Special Issue Research on Mitochondria and Cell Death in Disease Diagnosis and Treatment)

► Show Figures

Figure 1

13 pages, 2051 KiB

Open AccessReview

Atheroprotective Aspects of Heat Shock Proteins

by Anastasia V. Poznyak, Varvara A. Orekhova, Vasily N. Sukhorukov, Victoria A. Khotina, Mikhail A. Popov and Alexander N. Orekhov

Int. J. Mol. Sci. 2023, 24(14), 11750; https://doi.org/10.3390/ijms241411750 - 21 Jul 2023

Cited by 3 | Viewed by 1417

Abstract

Atherosclerosis is a major global health problem. Being a harbinger of a large number of cardiovascular diseases, it ultimately leads to morbidity and mortality. At the same time, effective measures for the prevention and treatment of atherosclerosis have not been developed, to date. All available therapeutic options have a number of limitations. To understand the mechanisms behind the triggering and development of atherosclerosis, a deeper understanding of molecular interactions is needed. Heat shock proteins are important for the normal functioning of cells, actively helping cells adapt to gradual changes in the environment and survive in deadly conditions. Moreover, multiple HSP families play various roles in the progression of cardiovascular disorders. Some heat shock proteins have been shown to have antiatherosclerotic effects, while the role of others remains unclear. In this review, we considered certain aspects of the antiatherosclerotic activity of a number of heat shock proteins. Full article

(This article belongs to the Special Issue Research on Mitochondria and Cell Death in Disease Diagnosis and Treatment)

► Show Figures

Figure 1

33 pages, 1370 KiB

Open AccessReview

Mitochondrial Transfer as a Novel Therapeutic Approach in Disease Diagnosis and Treatment

by Vicente Javier Clemente-Suárez, Alexandra Martín-Rodríguez, Rodrigo Yáñez-Sepúlveda and José Francisco Tornero-Aguilera

Int. J. Mol. Sci. 2023, 24(10), 8848; https://doi.org/10.3390/ijms24108848 - 16 May 2023

Cited by 34 | Viewed by 6861

Abstract

Mitochondrial dysfunction is a hallmark of numerous diseases, including neurodegenerative disorders, metabolic disorders, and cancer. Mitochondrial transfer, the transfer of mitochondria from one cell to another, has recently emerged as a potential therapeutic approach for restoring mitochondrial function in diseased cells. In this review, we summarize the current understanding of mitochondrial transfer, including its mechanisms, potential therapeutic applications, and impact on cell death pathways. We also discuss the future directions and challenges in the field of mitochondrial transfer as a novel therapeutic approach in disease diagnosis and treatment. Full article

(This article belongs to the Special Issue Research on Mitochondria and Cell Death in Disease Diagnosis and Treatment)

► Show Figures

Figure 1

Show export options Show export options

Select all

Export citation of selected articles as:

Displaying articles 1-12

Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Planned Paper I：The effects of metals on mitochondira and function-Prof. Debbie C. Crans

Planned Paper II：The survival factor GDF15 protects insulin producing beta-cells against metabolic stress via increased deamination of intracellular adenosine-Dr. Nils Welsh

Planned Paper III: Lovastatin Induces Apoptosis in Human Pancreatic Cancer Cells by Inhibiting Cholesterol Rafts in Cell Membrane and Mitochondria-Prof. Hiroki Kuniyasu

Planned Paper IV: Targeting mitochondrial metabolism in glioblastoma-Dr. Hans-Uwe Simon

Planned Paper V: Anti-tumoral activity of Iridio induced mitochondrial damage and anti-PD-L1 combination in NSCLC cancer-Dr. Francesco Sabbatino

Planned Paper VI: NETosis, oxidative stress, mitochondrial plasticity and PI3K-Akt-mTORC related glucose metabolic alterations in SLE immunocytes-Dr. H-T Lee, Dr. C-S Lin and Professor C-Y-Tsai(Submission date to be determined)

Journal Menu

Journal Browser

Research on Mitochondria and Cell Death in Disease Diagnosis and Treatment

Share This Special Issue

Special Issue Editor

Special Issue Information

Keywords

Benefits of Publishing in a Special Issue

Published Papers (12 papers)

Research

Review

Planned Papers

Further Information

Guidelines

MDPI Initiatives

Follow MDPI