Oxidative stress, antioxidants, hormesis and calorie restriction: The current perspective in the biology of aging

Mehdi, Mohammad Murtaza; Solanki, Preeti; Singh, Prabhakar

doi:10.1016/j.archger.2021.104413

Cited by 34 publications

(8 citation statements)

References 201 publications

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“…Cells are routinely exposed to aging-promoting stressors (e.g., chemical stress, thermal stress, and stress from UV exposure) and rely on protective mechanisms (e.g., DNA repair pathways, and heat shock proteins) to prevent macromolecule damage [ 4 ]. Oxidative stress, a condition caused by the imbalance between reactive oxygen species (ROS) and antioxidants that can neutralize them, occurs both extrinsically through chemical stress and intrinsically as byproducts of cellular metabolism [ 5 ]. While additional ROS in a state of oxidative stress can contribute to aging, ROS produced below a certain threshold are essential to stress and metabolic regulatory signaling pathways that maintain cellular homeostasis [ 1 ].…”

Section: Introductionmentioning

confidence: 99%

“…While additional ROS in a state of oxidative stress can contribute to aging, ROS produced below a certain threshold are essential to stress and metabolic regulatory signaling pathways that maintain cellular homeostasis [ 1 ]. Therefore, small amounts of stress may produce a hormetic effect and promote cellular survival [ 1 , 5 , 6 ]. Because cellular responses to intrinsic and extrinsic stress are highly interrelated and can create additive impacts on aging, “multiplex” stress resistance is likely required for slowing of the aging process [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

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Characterization of Stress Responses in a Drosophila Model of Werner Syndrome

et al. 2021

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As organisms age, their resistance to stress decreases while their risk of disease increases. This can be shown in patients with Werner syndrome (WS), which is a genetic disease characterized by accelerated aging along with increased risk of cancer and metabolic disease. WS is caused by mutations in WRN, a gene involved in DNA replication and repair. Recent research has shown that WRN mutations contribute to multiple hallmarks of aging including genomic instability, telomere attrition, and mitochondrial dysfunction. However, questions remain regarding the onset and effect of stress on early aging. We used a fly model of WS (WRNexoΔ) to investigate stress response during different life stages and found that stress sensitivity varies according to age and stressor. While larvae and young WRNexoΔ adults are not sensitive to exogenous oxidative stress, high antioxidant activity suggests high levels of endogenous oxidative stress. WRNexoΔ adults are sensitive to stress caused by elevated temperature and starvation suggesting abnormalities in energy storage and a possible link to metabolic dysfunction in WS patients. We also observed higher levels of sleep in aged WRNexoΔ adults suggesting an additional adaptive mechanism to protect against age-related stress. We suggest that stress response in WRNexoΔ is multifaceted and evokes a systemic physiological response to protect against cellular damage. These data further validate WRNexoΔ flies as a WS model with which to study mechanisms of early aging and provide a foundation for development of treatments for WS and similar diseases.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Characterization of Stress Responses in a Drosophila Model of Werner Syndrome

et al. 2021

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“…With respect to lifespan extension, one of the most studied current modes of intervention is the cellular rejuvenation process. In this context it is often proposed that through selective genetic modulation of longevity regulating factors a reversal of aging-related damage can be achieved [198,201]. Several prominent reports have indeed suggested that reversal of aging damage can occur, e.g., in vivo ectopic expression of three (Oct4, Sox2, Klf4) of the four Yamanaka reprogramming factors [202] was able to promote axon regeneration after previous eye injury [203] and also stem multiple aspects of aging-related disease such as renal failure, cardiomyopathies, and diabetic conditions [201].…”

Section: Discussionmentioning

confidence: 99%

The Relaxin-3 Receptor, RXFP3, Is a Modulator of Aging-Related Disease

Leysen

Walter

Clauwaert

et al. 2022

IJMS

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During the aging process our body becomes less well equipped to deal with cellular stress, resulting in an increase in unrepaired damage. This causes varying degrees of impaired functionality and an increased risk of mortality. One of the most effective anti-aging strategies involves interventions that combine simultaneous glucometabolic support with augmented DNA damage protection/repair. Thus, it seems prudent to develop therapeutic strategies that target this combinatorial approach. Studies have shown that the ADP-ribosylation factor (ARF) GTPase activating protein GIT2 (GIT2) acts as a keystone protein in the aging process. GIT2 can control both DNA repair and glucose metabolism. Through in vivo co-regulation analyses it was found that GIT2 forms a close coexpression-based relationship with the relaxin-3 receptor (RXFP3). Cellular RXFP3 expression is directly affected by DNA damage and oxidative stress. Overexpression or stimulation of this receptor, by its endogenous ligand relaxin 3 (RLN3), can regulate the DNA damage response and repair processes. Interestingly, RLN3 is an insulin-like peptide and has been shown to control multiple disease processes linked to aging mechanisms, e.g., anxiety, depression, memory dysfunction, appetite, and anti-apoptotic mechanisms. Here we discuss the molecular mechanisms underlying the various roles of RXFP3/RLN3 signaling in aging and age-related disorders.

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“…In conditions considered to be major risk factors for atherosclerotic cardiovascular disease (including diabetes, hypertension, dyslipidemia and smoking), reactive oxygen species (ROS) are at increased abundance in the vessel wall ( 21 ). The free radical theory of aging suggests that aging occurs when cells suffer lasting damage due to sustained attack by free radicals ( 22 ). Mitochondria and nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs) are the two major sources of ROS production in the cell ( 23 ).…”

Section: The Pro-atherosclerotic Properties Of Senescent Vsmcsmentioning

confidence: 99%

Senescence in Vascular Smooth Muscle Cells and Atherosclerosis

Zha

Zhuang

Yang

et al. 2022

Front. Cardiovasc. Med.

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Vascular smooth muscle cells (VSMCs) are the primary cell type involved in the atherosclerosis process; senescent VSMCs are observed in both aged vessels and atherosclerotic plaques. Factors associated with the atherosclerotic process, including oxidative stress, inflammation, and calcium-regulating factors, are closely linked to senescence in VSMCs. A number of experimental studies using traditional cellular aging markers have suggested that anti-aging biochemical agents could be used to treat atherosclerosis. However, doubt has recently been cast on such potential due to the increasingly apparent complexity of VSMCs status and an incomplete understanding of the role that these cells play in the atherosclerosis process, as well as a lack of specific or spectrum-limited cellular aging markers. The utility of anti-aging drugs in atherosclerosis treatment should be reevaluated. Promotion of a healthy lifestyle, exploring in depth the characteristics of each cell type associated with atherosclerosis, including VSMCs, and development of targeted drug delivery systems will ensure efficacy whilst evaluation of the safety and tolerability of drug use should be key aims of future anti-atherosclerosis research. This review summarizes the characteristics of VSMC senescence during the atherosclerosis process, the factors regulating this process, as well as an overview of progress toward the development and application of anti-aging drugs.

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Oxidative stress, antioxidants, hormesis and calorie restriction: The current perspective in the biology of aging

Cited by 34 publications

References 201 publications

Characterization of Stress Responses in a Drosophila Model of Werner Syndrome

Characterization of Stress Responses in a Drosophila Model of Werner Syndrome

The Relaxin-3 Receptor, RXFP3, Is a Modulator of Aging-Related Disease

Senescence in Vascular Smooth Muscle Cells and Atherosclerosis

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