scholarly journals Mitochondrial Sirtuins in Reproduction

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1047
Author(s):  
Giovanna Di Emidio ◽  
Stefano Falone ◽  
Paolo Giovanni Artini ◽  
Fernanda Amicarelli ◽  
Anna Maria D’Alessandro ◽  
...  
Keyword(s):  
Stress Responses ◽  
Metabolic Pathways ◽  
Redox Balance ◽  
Antioxidant Defenses ◽  
Metabolic Abnormalities ◽  
Female Reproduction ◽  
Mitochondrial Dysfunctions ◽  
Early Embryos ◽  
The Relationship

Mitochondria act as hubs of numerous metabolic pathways. Mitochondrial dysfunctions contribute to altering the redox balance and predispose to aging and metabolic alterations. The sirtuin family is composed of seven members and three of them, SIRT3-5, are housed in mitochondria. They catalyze NAD+-dependent deacylation and the ADP-ribosylation of mitochondrial proteins, thereby modulating gene expression and activities of enzymes involved in oxidative metabolism and stress responses. In this context, mitochondrial sirtuins (mtSIRTs) act in synergistic or antagonistic manners to protect from aging and aging-related metabolic abnormalities. In this review, we focus on the role of mtSIRTs in the biological competence of reproductive cells, organs, and embryos. Most studies are focused on SIRT3 in female reproduction, providing evidence that SIRT3 improves the competence of oocytes in humans and animal models. Moreover, SIRT3 protects oocytes, early embryos, and ovaries against stress conditions. The relationship between derangement of SIRT3 signaling and the imbalance of ROS and antioxidant defenses in testes has also been demonstrated. Very little is known about SIRT4 and SIRT5 functions in the reproductive system. The final goal of this work is to understand whether sirtuin-based signaling may be taken into account as potential targets for therapeutic applications in female and male infertility.

scholarly journals Mitochondrial Dysfunctions and Altered Metals Homeostasis: New Weapons to Counteract HCV-Related Oxidative Stress

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Mario Arciello ◽  
Manuele Gori ◽  
Clara Balsano
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Metabolic Pathways ◽  
Energy Production ◽  
Power Plants ◽  
Focal Point ◽  
Antioxidant Defenses ◽  
Host Organism ◽  
Mitochondrial Dysfunctions

The hepatitis C virus (HCV) infection produces several pathological effects in host organism through a wide number of molecular/metabolic pathways. Today it is worldwide accepted that oxidative stress actively participates in HCV pathology, even if the antioxidant therapies adopted until now were scarcely effective. HCV causes oxidative stress by a variety of processes, such as activation of prooxidant enzymes, weakening of antioxidant defenses, organelle damage, and metals unbalance. A focal point, in HCV-related oxidative stress onset, is the mitochondrial failure. These organelles, known to be the “power plants” of cells, have a central role in energy production, metabolism, and metals homeostasis, mainly copper and iron. Furthermore, mitochondria are direct viral targets, because many HCV proteins associate with them. They are the main intracellular free radicals producers and targets. Mitochondrial dysfunctions play a key role in the metal imbalance. This event, today overlooked, is involved in oxidative stress exacerbation and may play a role in HCV life cycle. In this review, we summarize the role of mitochondria and metals in HCV-related oxidative stress, highlighting the need to consider their deregulation in the HCV-related liver damage and in the antiviral management of patients.

scholarly journals Novel insights on targeting ferroptosis in cancer therapy

2020 ◽  
Vol 8 (1) ◽  
Author(s):  
Sipeng Zuo ◽  
Jie Yu ◽  
Hui Pan ◽  
Linna Lu
Keyword(s):  
Cell Death ◽  
Heart Disease ◽  
Cancer Therapy ◽  
Alzheimer Disease ◽  
Cellular Structure ◽  
Redox Balance ◽  
Regulated Cell Death ◽  
Novel Theory ◽  
The Relationship

Abstract Ferroptosis belongs to a novel form of regulated cell death. It is characterized by iron dependence, destruction of intracellular redox balance and non-apoptosis. And cellular structure and molecules level changes also occur abnormally during ferroptosis. It has been proved that ferroptosis exist widespreadly in many diseases, such as heart disease, brain damage or alzheimer disease. At the same time, the role of ferroptosis in cancer cannot be underestimated. More and more indications have told that ferroptosis is becoming a powerful weapon against cancer. In addition, therapies rely on ferroptosis have been applied to the clinic. Therefore, it is necessary to understand this newly discovered form of cell death and its connection with cancer. This review summarizes the mechanism of ferroptosis, ferroptosis inducers based on different targets and inspection methods. At last, we analyzed the relationship between ferroptosis and malignancies, in order to provide a novel theory basis for cancer treatment.

scholarly journals The Role of Oxidative Stress, Mitochondrial Function, and Autophagy in Diabetic Polyneuropathy

2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Sonia Sifuentes-Franco ◽  
Fermín Paul Pacheco-Moisés ◽  
Adolfo Daniel Rodríguez-Carrizalez ◽  
Alejandra Guillermina Miranda-Díaz
Keyword(s):  
Oxidative Stress ◽  
Metabolic Pathways ◽  
Metabolic Diseases ◽  
Mitochondrial Fission ◽  
Diabetic Polyneuropathy ◽  
Stress Factors ◽  
Antioxidant Defenses ◽  
Stress Hyperglycemia ◽  
Antioxidant Agents

Diabetic polyneuropathy (DPN) is the most frequent and prevalent chronic complication of diabetes mellitus (DM). The state of persistent hyperglycemia leads to an increase in the production of cytosolic and mitochondrial reactive oxygen species (ROS) and favors deregulation of the antioxidant defenses that are capable of activating diverse metabolic pathways which trigger the presence of nitro-oxidative stress (NOS) and endoplasmic reticulum stress. Hyperglycemia provokes the appearance of micro- and macrovascular complications and favors oxidative damage to the macromolecules (lipids, carbohydrates, and proteins) with an increase in products that damage the DNA. Hyperglycemia produces mitochondrial dysfunction with deregulation between mitochondrial fission/fusion and regulatory factors. Mitochondrial fission appears early in diabetic neuropathy with the ability to facilitate mitochondrial fragmentation. Autophagy is a catabolic process induced by oxidative stress that involves the formation of vesicles by the lysosomes. Autophagy protects cells from diverse stress factors and routine deterioration. Clarification of the mechanisms involved in the appearance of complications in DM will facilitate the selection of specific therapeutic options based on the mechanisms involved in the metabolic pathways affected. Nowadays, the antioxidant agents consumed exogenously form an adjuvant therapeutic alternative in chronic degenerative metabolic diseases, such as DM.

scholarly journals Metabolic Regulation of Redox Balance in Cancer

Cancers ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 955 ◽  
Author(s):  
Vinee Purohit ◽  
Diane M. Simeone ◽  
Costas A. Lyssiotis
Keyword(s):  
Metabolic Pathways ◽  
Metabolic Regulation ◽  
Redox Homeostasis ◽  
Redox Balance ◽  
Tumor Evolution ◽  
Ros Production ◽  
Oxygen Species ◽  
Partial Reduction ◽  
Dna Mutations

Reactive oxygen species (ROS) are chemically active free radicals produced by partial reduction of oxygen that can activate discrete signaling pathways or disrupt redox homeostasis depending on their concentration. ROS interacts with biomolecules, including DNA, and can cause mutations that can transform normal cells into cancer cells. Furthermore, certain cancer-causing mutations trigger alterations in cellular metabolism that can increase ROS production, resulting in genomic instability, additional DNA mutations, and tumor evolution. To prevent excess ROS-mediated toxicity, cancer-causing mutations concurrently activate pathways that manage this oxidative burden. Hence, an understanding of the metabolic pathways that regulate ROS levels is imperative for devising therapies that target tumor cells. In this review, we summarize the dual role of metabolism as a generator and inhibitor of ROS in cancer and discuss current strategies to target the ROS axis.

scholarly journals Role of Reductive versus Oxidative Stress in Tumor Progression and Anticancer Drug Resistance

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 758
Author(s):  
Kyung-Soo Chun ◽  
Do-Hee Kim ◽  
Young-Joon Surh
Keyword(s):  
Cancer Cells ◽  
Metabolic Pathways ◽  
Redox Homeostasis ◽  
Redox Balance ◽  
Therapy Resistance ◽  
Related Factor ◽  
Nuclear Factor ◽  
Cellular Redox ◽  
Reductive Stress

Redox homeostasis is not only essential for the maintenance of normal physiological functions, but also plays an important role in the growth, survival, and therapy resistance of cancer cells. Altered redox balance and consequent disruption of redox signaling are implicated in the proliferation and progression of cancer cells and their resistance to chemo- and radiotherapy. The nuclear factor erythroid 2 p45-related factor (Nrf2) is the principal stress-responsive transcription factor that plays a pivotal role in maintaining cellular redox homeostasis. Aberrant Nrf2 overactivation has been observed in many cancerous and transformed cells. Uncontrolled amplification of Nrf2-mediated antioxidant signaling results in reductive stress. Some metabolic pathways altered due to reductive stress have been identified as major contributors to tumorigenesis. This review highlights the multifaceted role of reductive stress in cancer development and progression.

scholarly journals Emerging Role of TCA Cycle-Related Enzymes in Human Diseases

2021 ◽  
Vol 22 (23) ◽  
pp. 13057
Author(s):  
Woojin Kang ◽  
Miki Suzuki ◽  
Takako Saito ◽  
Kenji Miyado
Keyword(s):  
Metabolic Pathways ◽  
Tca Cycle ◽  
Tricarboxylic Acid ◽  
Human Diseases ◽  
Comprehensive Overview ◽  
Cellular Energy ◽  
Neurometabolic Disorders ◽  
Related Enzyme ◽  
The Relationship

The tricarboxylic acid (TCA) cycle is the main source of cellular energy and participates in many metabolic pathways in cells. Recent reports indicate that dysfunction of TCA cycle-related enzymes causes human diseases, such as neurometabolic disorders and tumors, have attracted increasing interest in their unexplained roles. The diseases which develop as a consequence of loss or dysfunction of TCA cycle-related enzymes are distinct, suggesting that each enzyme has a unique function. This review aims to provide a comprehensive overview of the relationship between each TCA cycle-related enzyme and human diseases. We also discuss their functions in the context of both mitochondrial and extra-mitochondrial (or cytoplasmic) enzymes.

scholarly journals Metabolic Control of Epilepsy: A Promising Therapeutic Target for Epilepsy

2020 ◽  
Vol 11 ◽  
Author(s):  
Yanqing Fei ◽  
Ruting Shi ◽  
Zhi Song ◽  
Jinze Wu
Keyword(s):  
Metabolic Pathways ◽  
Brain Metabolism ◽  
Dietary Therapy ◽  
Metabolic Characteristics ◽  
Neuronal Excitation ◽  
Metabolic Defects ◽  
Promising Therapeutic Target ◽  
Drug Resistant Epilepsy ◽  
The Relationship

Epilepsy is a common neurological disease that is not always controlled, and the ketogenic diet shows good antiepileptic effects drug-resistant epilepsy or seizures caused by specific metabolic defects via regulating the metabolism. The brain is a vital organ with high metabolic demands, and epileptic foci tend to exhibit high metabolic characteristics. Accordingly, there has been growing interest in the relationship between brain metabolism and epilepsy in recent years. To date, several new antiepileptic therapies targeting metabolic pathways have been proposed (i.e., inhibiting glycolysis, targeting lactate dehydrogenase, and dietary therapy). Promising strategies to treat epilepsy via modulating the brain's metabolism could be expected, while a lack of thorough understanding of the role of brain metabolism in the control of epilepsy remains. Herein, this review aims to provide insight into the state of the art concerning the brain's metabolic patterns and their association with epilepsy. Regulation of neuronal excitation via metabolic pathways and antiepileptic therapies targeting metabolic pathways are emphasized, which could provide a better understanding of the role of metabolism in epilepsy and could reveal potential therapeutic targets.

scholarly journals Depression as a Failed Anxiety: The Continuum of Precision-Weighting Dysregulation in Affective Disorders

2021 ◽  
Vol 12 ◽  
Author(s):  
Valery Krupnik
Keyword(s):  
Stress Response ◽  
Stress Responses ◽  
Affective Disorders ◽  
Predictive Processing ◽  
Anxiety And Depression ◽  
Depression Symptoms ◽  
High Anxiety ◽  
The Relationship ◽  
The Continuum

Depressive, anxiety, and trauma-related disorders have many symptoms in common such as unstable mood, high anxiety, sleep disturbance, impaired concentration among others. This degeneracy creates ambiguity in classifying psychiatric disorders and raises the question of their categorical vs. dimensional nature. Consequently, such ambiguity presents a dilemma for choosing diagnosis-specific vs. trans-diagnostic therapies. In this paper, I build on a theory that considers affective disorders on the continuum of stress response from normative to traumatic. Using an integrative evolutionary-stress response-predictive processing (iESP) model, I arrange affective disorders on a continuum of precision-weighting dysregulation, where depressive, anxiety and trauma-induced disorders have a characteristic pattern of precision-weighting dysregulation. I specifically address the relationship between anxiety and depressive stress responses, exploring the role of anxiety in the dynamics of depressive stress response and the resulting high co-occurrence of anxiety and depression symptoms. Finally, I discuss the model's relevance for therapy of depression.

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