Mitochondria hormesis delays aging and associated diseases in Caenorhabditis elegans impacting on key ferroptosis players

Schiavi, Alfonso; Salveridou, Eva; Brinkmann, Vanessa; Shaik, Anjumara; Menzel, Ralph; Kalyanasundaram, Sumana; Nygård, Ståle; Nilsen, Hilde; Ventura, Natascia

doi:10.1016/j.isci.2023.106448

Cited by 4 publications

(3 citation statements)

References 94 publications

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“…Additionally, the combination of increased resistance to oxidative and thermal stress displayed by the worms, coupled with enhanced body bending, is frequently associated with the concept of hormesis [ 34 , 35 ]. This phenomenon forms the basis of various pro-longevity interventions, encompassing fasting, dietary restriction, and controlled exposure to stressors [ 34 , 35 , 36 , 37 ]. Furthermore, studies conducted on model organisms report the existence of plant-derived molecules that mimic the effects of mild stressors, such as dietary restriction, resulting in reduced lipid accumulation concurrently with improved stress resistance and subsequent extension of lifespan [ 10 ].…”

Section: Resultsmentioning

confidence: 99%

Icariin Improves Stress Resistance and Extends Lifespan in Caenorhabditis elegans through hsf-1 and daf-2-Driven Hormesis

Todorova,

Savova,

Mihaylova

et al. 2023

IJMS

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Aging presents an increasingly significant challenge globally, driven by the growing proportion of individuals aged 60 and older. Currently, there is substantial research interest in pro-longevity interventions that target pivotal signaling pathways, aiming not only to extend lifespan but also to enhance healthspan. One particularly promising approach involves inducing a hormetic response through the utilization of natural compounds defined as hormetins. Various studies have introduced the flavonoid icariin as beneficial for age-related diseases such as cardiovascular and neurodegenerative conditions. To validate its potential pro-longevity properties, we employed Caenorhabditis elegans as an experimental platform. The accumulated results suggest that icariin extends the lifespan of C. elegans through modulation of the DAF-2, corresponding to the insulin/IGF-1 signaling pathway in humans. Additionally, we identified increased resistance to heat and oxidative stress, modulation of lipid metabolism, improved late-life healthspan, and an extended lifespan upon icariin treatment. Consequently, a model mechanism of action was provided for icariin that involves the modulation of various players within the stress-response network. Collectively, the obtained data reveal that icariin is a potential hormetic agent with geroprotective properties that merits future developments.

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Section: Resultsmentioning

confidence: 99%

Icariin Improves Stress Resistance and Extends Lifespan in Caenorhabditis elegans through hsf-1 and daf-2-Driven Hormesis

Todorova,

Savova,

Mihaylova

et al. 2023

IJMS

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“…The authors suggest that part of this mechanism involves the mitigation of ferroptosis, a type of non-apoptotic cell death triggered by iron-induced lipid peroxidation. This mitigation occurs through interactions with various essential components of ferroptosis and is likely facilitated by the independence of the enzyme GPx redox system [129].…”

Section: Iron and Cuppermentioning

confidence: 99%

Mitochondria in the Spotlight: C. elegans as a Model Organism to Evaluate Xenobiotic-Induced Dysfunction

Martins,

Virgolini,

Ávila

et al. 2023

Cells

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Mitochondria play a crucial role in cellular respiration, ATP production, and the regulation of various cellular processes. Mitochondrial dysfunctions have been directly linked to pathophysiological conditions, making them a significant target of interest in toxicological research. In recent years, there has been a growing need to understand the intricate effects of xenobiotics on human health, necessitating the use of effective scientific research tools. Caenorhabditis elegans (C. elegans), a nonpathogenic nematode, has emerged as a powerful tool for investigating toxic mechanisms and mitochondrial dysfunction. With remarkable genetic homology to mammals, C. elegans has been used in studies to elucidate the impact of contaminants and drugs on mitochondrial function. This review focuses on the effects of several toxic metals and metalloids, drugs of abuse and pesticides on mitochondria, highlighting the utility of C. elegans as a model organism to investigate mitochondrial dysfunction induced by xenobiotics. Mitochondrial structure, function, and dynamics are discussed, emphasizing their essential role in cellular viability and the regulation of processes such as autophagy, apoptosis, and calcium homeostasis. Additionally, specific toxins and toxicants, such as arsenic, cadmium, and manganese are examined in the context of their impact on mitochondrial function and the utility of C. elegans in elucidating the underlying mechanisms. Furthermore, we demonstrate the utilization of C. elegans as an experimental model providing a promising platform for investigating the intricate relationships between xenobiotics and mitochondrial dysfunction. This knowledge could contribute to the development of strategies to mitigate the adverse effects of contaminants and drugs of abuse, ultimately enhancing our understanding of these complex processes and promoting human health.

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“…Due to involving various and complicated signaling, ferroptosis plays an important role in the occurrence and development of major chronic diseases and different roles in different disease contexts. A growing body of evidence suggests that the imbalance of ferroptosis affects, development and aging [ 13 , 14 ], and is closely related to the tumor [ 8 , 15 , 16 ], ischemic diseases [ 17 – 22 ], neurodegenerative disease [ 23 , 24 ], organ transplantation [ 25 , 26 ], cardiovascular disease [ 27 – 29 ], autoimmune functions [ 15 , 30 ], infection [ 31 , 32 ], iron-overload disease [ 33 ], and so on (Fig. 2 ).…”

Section: Introductionmentioning

confidence: 99%

The mechanism of ferroptosis and its related diseases

Feng,

Tang,

Wang

et al. 2023

Mol Biomed

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Ferroptosis, a regulated form of cellular death characterized by the iron-mediated accumulation of lipid peroxides, provides a novel avenue for delving into the intersection of cellular metabolism, oxidative stress, and disease pathology. We have witnessed a mounting fascination with ferroptosis, attributed to its pivotal roles across diverse physiological and pathological conditions including developmental processes, metabolic dynamics, oncogenic pathways, neurodegenerative cascades, and traumatic tissue injuries. By unraveling the intricate underpinnings of the molecular machinery, pivotal contributors, intricate signaling conduits, and regulatory networks governing ferroptosis, researchers aim to bridge the gap between the intricacies of this unique mode of cellular death and its multifaceted implications for health and disease. In light of the rapidly advancing landscape of ferroptosis research, we present a comprehensive review aiming at the extensive implications of ferroptosis in the origins and progress of human diseases. This review concludes with a careful analysis of potential treatment approaches carefully designed to either inhibit or promote ferroptosis. Additionally, we have succinctly summarized the potential therapeutic targets and compounds that hold promise in targeting ferroptosis within various diseases. This pivotal facet underscores the burgeoning possibilities for manipulating ferroptosis as a therapeutic strategy. In summary, this review enriched the insights of both investigators and practitioners, while fostering an elevated comprehension of ferroptosis and its latent translational utilities. By revealing the basic processes and investigating treatment possibilities, this review provides a crucial resource for scientists and medical practitioners, aiding in a deep understanding of ferroptosis and its effects in various disease situations.

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Mitochondria hormesis delays aging and associated diseases in Caenorhabditis elegans impacting on key ferroptosis players

Cited by 4 publications

References 94 publications

Icariin Improves Stress Resistance and Extends Lifespan in Caenorhabditis elegans through hsf-1 and daf-2-Driven Hormesis

Icariin Improves Stress Resistance and Extends Lifespan in Caenorhabditis elegans through hsf-1 and daf-2-Driven Hormesis

Mitochondria in the Spotlight: C. elegans as a Model Organism to Evaluate Xenobiotic-Induced Dysfunction

The mechanism of ferroptosis and its related diseases

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