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Remodeling of Mitochondria in Cancer and Other Diseases

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

Deadline for manuscript submissions: closed (30 September 2021) | Viewed by 33314

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Special Issue Editors

Dr. Yong Teng

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Guest Editor

Department of Hematology and Medical Oncology, Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA 30322, USA
Interests: metastasis; molecular pathway; cancer models; metabolism; tumor microenvironment; drug screening and development
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Prof. Amadou K.S. Camara

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Guest Editor

Department of Anesthesiology and Anesthesia Research, Medical College of Wisconsin, Milwaukee, WI, USA
Interests: mitochondria; mitochondrial calcium regulation; voltage dependent anion channel; hexokinase; adenine nucleotide translocator; ischemia and reperfusion; reactive oxygen and nitrogen species; hypothermia; traumatic brain injury
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Dr. Xin Qi

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Guest Editor

Department of Physiology and Biophysics, CASE School of Medicine, Cleveland, OH, USA

Special Issue Information

Mitochondria are highly dynamic and responsive organelles that are capable of undergoing fission and fusion and are the hub for diverse signal processors, which are fundamental to cellular homeostasis, energy production, metabolism, survival, and death. Mitochondiral remodeling, including rearranging, recycling, and reprogramming, is essential for mitochondrial quality control, structural integrity, and functional interaction with other cellular organelles. Alhtough we are still far from fully understanding the complexity of mitochondrial remodeling in its physiological and pathophysiological significance, this process has been, nonetheless, implicated in the pathogenesis of many human disorders, including cancer and aging-related diseases. With the advent of new information, technologies, and methodologies, it is time to delineate the significance and enigmatic mechanisms relevant to the dynamic remodeling of mitochondria in response to pathophysiological stresses in a more precise and comprehensive way. In this respect, scientific evidence and provocative ideas are important to translate science into practice effectively. Therefore, we kindly invite you to contribute to this Special Issue with original research articles or comprehensive reviews on all molecular aspects related to the theme of “Remodeling of Mitochondria in Cancer and Other Diseases”. Short perspective papers or pure clinical papers will not be considered, while novel Communication articles with interesting molecular data will be of interest. This Special Issue aims to increase our understanding of the role, regulation, and impact of mitochondrial remodeling in disease-specific pathology and possibly translate these finding into therapeutics, from basic research to the clinic.

Prof. Amadou K.S. Camara
Dr. Xin Qi
Dr. Yong Teng
Guest Editors

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Keywords

Mitochondrial biology
mitochondrial remodeling
mitochondrial biogenesis and bioenergetics
mitochondrial dynamic network
cancer development and progression
mitochodria-associated human diseases
mitochondria communication
targeting mitochondria
mitochondrial oncolgoy

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Related Special Issue

Remodeling of Mitochondria in Cancer and Other Diseases 2.0 in International Journal of Molecular Sciences (1 article)

Published Papers (9 papers)

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Editorial

Jump to: Research, Review

3 pages, 191 KiB

Open AccessEditorial

Remodeling of Mitochondria in Cancer and Other Diseases

by Yong Teng

Int. J. Mol. Sci. 2023, 24(9), 7693; https://doi.org/10.3390/ijms24097693 - 22 Apr 2023

Cited by 2 | Viewed by 1771

Abstract

Mitochondria are highly dynamic and responsive organelles capable of fission and fusion and are a hub of diverse signaling pathways that are fundamental to cellular homeostasis, energy production, metabolism, survival, and death [...] Full article

(This article belongs to the Special Issue Remodeling of Mitochondria in Cancer and Other Diseases)

Research

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21 pages, 2536 KiB

Open AccessArticle

Platelet Mitochondrial Bioenergetics Reprogramming in Patients with Urothelial Carcinoma

by Patrik Palacka, Anna Gvozdjáková, Zuzana Rausová, Jarmila Kucharská, Ján Slopovský, Jana Obertová, Daniel Furka, Samuel Furka, Keshav K. Singh and Zuzana Sumbalová

Int. J. Mol. Sci. 2022, 23(1), 388; https://doi.org/10.3390/ijms23010388 - 30 Dec 2021

Cited by 11 | Viewed by 2907

Abstract

Mitochondrial bioenergetics reprogramming is an essential response of cells to stress. Platelets, an accessible source of mitochondria, have a crucial role in cancer development; however, the platelet mitochondrial function has not been studied in urothelial carcinoma (UC) patients. A total of 15 patients with UC and 15 healthy controls were included in the study. Parameters of platelet mitochondrial respiration were evaluated using the high-resolution respirometry method, and the selected antioxidant levels were determined by HPLC. In addition, oxidative stress was evaluated by the thiobarbituric acid reactive substances (TBARS) concentration in plasma. We demonstrated deficient platelet mitochondrial respiratory chain functions, oxidative phosphorylation (OXPHOS), and electron transfer (ET) capacity with complex I (CI)-linked substrates, and reduced the endogenous platelet coenzyme Q₁₀ (CoQ₁₀) concentration in UC patients. The activity of citrate synthase was decreased in UC patients vs. controls (p = 0.0191). γ-tocopherol, α-tocopherol in platelets, and β-carotene in plasma were significantly lower in UC patients (p = 0.0019; p = 0.02; p = 0.0387, respectively), whereas the plasma concentration of TBARS was increased (p = 0.0022) vs. controls. The changes in platelet mitochondrial bioenergetics are consistent with cell metabolism reprogramming in UC patients. We suppose that increased oxidative stress, decreased OXPHOS, and a reduced platelet endogenous CoQ₁₀ level can contribute to the reprogramming of platelet mitochondrial OXPHOS toward the activation of glycolysis. The impaired mitochondrial function can contribute to increased oxidative stress by triggering the reverse electron transport from the CoQ₁₀ cycle (Q-junction) to CI. Full article

(This article belongs to the Special Issue Remodeling of Mitochondria in Cancer and Other Diseases)

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15 pages, 3039 KiB

Open AccessArticle

Exploration of the Cytoplasmic Function of Abnormally Fertilized Embryos via Novel Pronuclear-Stage Cytoplasmic Transfer

by Ayako Fujimine-Sato, Takashi Kuno, Keiko Higashi, Atsushi Sugawara, Hiroaki Hiraga, Aiko Takahashi, Keiko Tanaka, Emi Yokoyama, Naomi Shiga, Zen Watanabe, Nobuo Yaegashi and Masahito Tachibana

Int. J. Mol. Sci. 2021, 22(16), 8765; https://doi.org/10.3390/ijms22168765 - 16 Aug 2021

Cited by 2 | Viewed by 3069

Abstract

In regular IVF, a portion of oocytes exhibit abnormal numbers of pronuclei (PN) that is considered as abnormal fertilization, and they are routinely discarded. However, it is known that abnormal ploidy still does not completely abandon embryo development and implantation. To explore the potential of cytoplasm from those abnormally fertilized oocytes, we developed a novel technique for the transfer of large cytoplasm between pronuclear-stage mouse embryos, and assessed its impact. A large volume of cytoplast could be efficiently transferred in the PN stage using a novel two-step method of pronuclear-stage cytoplasmic transfer (PNCT). PNCT revealed the difference in the cytoplasmic function among abnormally fertilized embryos where the cytoplasm of 3PN was developmentally more competent than 1PN, and the supplementing of fresh 3PN cytoplasm restored the impaired developmental potential of postovulatory “aged” oocytes. PNCT-derived embryos harbored significantly higher mitochondrial DNA copies, ATP content, oxygen consumption rate, and total cells. The difference in cytoplasmic function between 3PN and 1PN mouse oocytes probably attributed to the proper activation via sperm and may impact subsequent epigenetic events. These results imply that PNCT may serve as a potential alternative treatment to whole egg donation for patients with age-related recurrent IVF failure. Full article

(This article belongs to the Special Issue Remodeling of Mitochondria in Cancer and Other Diseases)

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21 pages, 8101 KiB

Open AccessArticle

No Direct Postconditioning Effect of Poloxamer 188 on Mitochondrial Function after Ischemia Reperfusion Injury in Rat Isolated Hearts

by Josephine Eskaf, William J. Cleveland and Matthias L. Riess

Int. J. Mol. Sci. 2021, 22(9), 4879; https://doi.org/10.3390/ijms22094879 - 5 May 2021

Cited by 5 | Viewed by 2088

Abstract

Myocardial infarction is a leading cause for morbidity and mortality worldwide. The only viable treatment for the ischemic insult is timely reperfusion, which further exacerbates myocardial injury. Maintaining mitochondrial function is crucial in preserving cardiomyocyte function in ischemia reperfusion (IR) injury. Poloxamer (P) 188 has been shown to improve cardiac IR injury by improving cellular and mitochondrial function. The aim of this study was to show if P188 postconditioning has direct protective effects on mitochondrial function in the heart. Langendorff prepared rat hearts were subjected to IR injury ex-vivo and reperfused for 10 min with 1 mM P188 vs. vehicle. Cardiac mitochondria were isolated with 1 mM P188 vs. 1 mM polyethylene glycol (PEG) vs. vehicle by differential centrifugation. Mitochondrial function was assessed by adenosine triphosphate synthesis, oxygen consumption, and calcium retention capacity. Mitochondrial function decreased significantly after ischemia and showed mild improvement with reperfusion. P188 did not improve mitochondrial function in the ex-vivo heart, and neither further P188 nor PEG induced direct mitochondrial protection after IR injury in this model. Full article

(This article belongs to the Special Issue Remodeling of Mitochondria in Cancer and Other Diseases)

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20 pages, 3623 KiB

Open AccessArticle

Mitochondrial Transfer Improves Cardiomyocyte Bioenergetics and Viability in Male Rats Exposed to Pregestational Diabetes

by Eli J. Louwagie, Tricia D. Larsen, Angela L. Wachal, Tyler C.T. Gandy and Michelle L. Baack

Int. J. Mol. Sci. 2021, 22(5), 2382; https://doi.org/10.3390/ijms22052382 - 27 Feb 2021

Cited by 31 | Viewed by 3793

Abstract

Offspring born to diabetic or obese mothers have a higher lifetime risk of heart disease. Previously, we found that rat offspring exposed to late-gestational diabetes mellitus (LGDM) and maternal high-fat (HF) diet develop mitochondrial dysfunction, impaired cardiomyocyte bioenergetics, and cardiac dysfunction at birth and again during aging. Here, we compared echocardiography, cardiomyocyte bioenergetics, oxidative damage, and mitochondria-mediated cell death among control, pregestational diabetes mellitus (PGDM)-exposed, HF-diet-exposed, and combination-exposed newborn offspring. We hypothesized that PGDM exposure, similar to LGDM, causes mitochondrial dysfunction to play a central, pathogenic role in neonatal cardiomyopathy. We found that PGDM-exposed offspring, similar to LGDM-exposed offspring, have cardiac dysfunction at birth, but their isolated cardiomyocytes have seemingly less bioenergetics impairment. This finding was due to confounding by impaired viability related to poorer ATP generation, more lipid peroxidation, and faster apoptosis under metabolic stress. To mechanistically isolate and test the role of mitochondria, we transferred mitochondria from normal rat myocardium to control and exposed neonatal rat cardiomyocytes. As expected, transfer provides a respiratory boost to cardiomyocytes from all groups. They also reduce apoptosis in PGDM-exposed males, but not in females. Findings highlight sex-specific differences in mitochondria-mediated mechanisms of developmentally programmed heart disease and underscore potential caveats of therapeutic mitochondrial transfer. Full article

(This article belongs to the Special Issue Remodeling of Mitochondria in Cancer and Other Diseases)

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19 pages, 26548 KiB

Open AccessArticle

Lifelong Ulk1-Mediated Autophagy Deficiency in Muscle Induces Mitochondrial Dysfunction and Contractile Weakness

by Anna S. Nichenko, Jacob R. Sorensen, W. Michael Southern, Anita E. Qualls, Albino G. Schifino, Jennifer McFaline-Figueroa, Jamie E. Blum, Kayvan F. Tehrani, Hang Yin, Luke J. Mortensen, Anna E. Thalacker-Mercer, Sarah M. Greising and Jarrod A. Call

Int. J. Mol. Sci. 2021, 22(4), 1937; https://doi.org/10.3390/ijms22041937 - 16 Feb 2021

Cited by 20 | Viewed by 3899

Abstract

The accumulation of damaged mitochondria due to insufficient autophagy has been implicated in the pathophysiology of skeletal muscle aging. Ulk1 is an autophagy-related kinase that initiates autophagosome assembly and may also play a role in autophagosome degradation (i.e., autophagy flux), but the contribution of Ulk1 to healthy muscle aging is unclear. Therefore, the purpose of this study was to investigate the role of Ulk1-mediated autophagy in skeletal muscle aging. At age 22 months (80% survival rate), muscle contractile and metabolic function were assessed using electrophysiology in muscle-specific Ulk1 knockout mice (MKO) and their littermate controls (LM). Specific peak-isometric torque of the ankle dorsiflexors (normalized by tibialis anterior muscle cross-sectional area) and specific force of the fast-twitch extensor digitorum longus muscles was reduced in MKO mice compared to LM mice (p < 0.03). Permeabilized muscle fibers from MKO mice had greater mitochondrial content, yet lower mitochondrial oxygen consumption and greater reactive oxygen species production compared to fibers from LM mice (p ≤ 0.04). Alterations in neuromuscular junction innervation patterns as well as changes to autophagosome assembly and flux were explored as possible contributors to the pathological features in Ulk1 deficiency. Of primary interest, we found that Ulk1 phosphorylation (activation) to total Ulk1 protein content was reduced in older muscles compared to young muscles from both human and mouse, which may contribute to decreased autophagy flux and an accumulation of dysfunctional mitochondria. Results from this study support the role of Ulk1-mediated autophagy in aging skeletal muscle, reflecting Ulk1′s dual role in maintaining mitochondrial integrity through autophagosome assembly and degradation. Full article

(This article belongs to the Special Issue Remodeling of Mitochondria in Cancer and Other Diseases)

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Review

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30 pages, 1361 KiB

Open AccessReview

Mitochondria: Insights into Crucial Features to Overcome Cancer Chemoresistance

by Ilaria Genovese, Marianna Carinci, Lorenzo Modesti, Gianluca Aguiari, Paolo Pinton and Carlotta Giorgi

Int. J. Mol. Sci. 2021, 22(9), 4770; https://doi.org/10.3390/ijms22094770 - 30 Apr 2021

Cited by 37 | Viewed by 5882

Abstract

Mitochondria are key regulators of cell survival and are involved in a plethora of mechanisms, such as metabolism, Ca²⁺ signaling, reactive oxygen species (ROS) production, mitophagy and mitochondrial transfer, fusion, and fission (known as mitochondrial dynamics). The tuning of these processes in pathophysiological conditions is fundamental to the balance between cell death and survival. Indeed, ROS overproduction and mitochondrial Ca²⁺ overload are linked to the induction of apoptosis, while the impairment of mitochondrial dynamics and metabolism can have a double-faceted role in the decision between cell survival and death. Tumorigenesis involves an intricate series of cellular impairments not yet completely clarified, and a further level of complexity is added by the onset of apoptosis resistance mechanisms in cancer cells. In the majority of cases, cancer relapse or lack of responsiveness is related to the emergence of chemoresistance, which may be due to the cooperation of several cellular protection mechanisms, often mitochondria-related. With this review, we aim to critically report the current evidence on the relationship between mitochondria and cancer chemoresistance with a particular focus on the involvement of mitochondrial dynamics, mitochondrial Ca²⁺ signaling, oxidative stress, and metabolism to possibly identify new approaches or targets for overcoming cancer resistance. Full article

(This article belongs to the Special Issue Remodeling of Mitochondria in Cancer and Other Diseases)

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18 pages, 2211 KiB

Open AccessReview

Structural and Functional Remodeling of Mitochondria in Cardiac Diseases

by Xiaonan Sun, Jalen Alford and Hongyu Qiu

Int. J. Mol. Sci. 2021, 22(8), 4167; https://doi.org/10.3390/ijms22084167 - 17 Apr 2021

Cited by 23 | Viewed by 4272

Abstract

Mitochondria undergo structural and functional remodeling to meet the cell demand in response to the intracellular and extracellular stimulations, playing an essential role in maintaining normal cellular function. Merging evidence demonstrated that dysregulation of mitochondrial remodeling is a fundamental driving force of complex human diseases, highlighting its crucial pathophysiological roles and therapeutic potential. In this review, we outlined the progress of the molecular basis of mitochondrial structural and functional remodeling and their regulatory network. In particular, we summarized the latest evidence of the fundamental association of impaired mitochondrial remodeling in developing diverse cardiac diseases and the underlying mechanisms. We also explored the therapeutic potential related to mitochondrial remodeling and future research direction. This updated information would improve our knowledge of mitochondrial biology and cardiac diseases’ pathogenesis, which would inspire new potential strategies for treating these diseases by targeting mitochondria remodeling. Full article

(This article belongs to the Special Issue Remodeling of Mitochondria in Cancer and Other Diseases)

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14 pages, 1038 KiB

Open AccessReview

Emerging Links between Control of Mitochondrial Protein ATAD3A and Cancer

by Liwei Lang, Reid Loveless and Yong Teng

Int. J. Mol. Sci. 2020, 21(21), 7917; https://doi.org/10.3390/ijms21217917 - 25 Oct 2020

Cited by 28 | Viewed by 4277

Abstract

Spanning from the mitochondria’s outer surface to the inner membrane, the nuclear-encoded protein ATAD3A maintains vital roles in regulating mitochondrial dynamics, homeostasis, metabolism, and interactions with the endoplasmic reticulum. Recently, elevated levels of ATAD3A have been reported in several types of cancer and to be tightly correlated with cancer development and progression, including increased cancer cell potential of proliferation, metastasis, and resistance to chemotherapy and radiotherapy. In the current review, we reveal ATAD3A as the link between mitochondrial functions and cancer biology and the accumulating evidence presenting ATAD3A as an attractive target for the development of novel cancer therapy to inhibit aberrant cancer metabolism and progression. Full article

(This article belongs to the Special Issue Remodeling of Mitochondria in Cancer and Other Diseases)

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