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Antioxidants
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ROS in Aging and Age-Related Disease
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ROS in Aging and Age-Related Disease

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (30 April 2022) | Viewed by 65181

Special Issue Editor

Dr. Ana L. Santos

E-Mail Website
Guest Editor
1. Department of Chemistry, Rice University, Houston, TX, USA
2. IdISBA - Fundación de Investigación Sanitaria de las Islas Baleares, Palma, Spain
Interests: oxidative stress; antioxidants; aging; communicable and non-communicable diseases; antimicrobials

Special Issue Information

Reactive oxygen species (ROS) are a natural byproduct of aerobic cellular metabolism. At physiological levels, ROS regulate multiple cellular processes including cell signaling and host defenses, and are kept in check by enzymatic (e.g., dismutases and peroxidases) and non-enzymatic (e.g., vitamin E and glutathione) antioxidants. When the levels of ROS overwhelm antioxidant defenses, oxidative stress ensues, resulting in oxidative damage to nucleic acids, proteins, and lipids.

The involvement of ROS in aging was first proposed by Harman’s “Free Radical Theory of Aging” in 1956, according to which aging and aging-associated diseases are the result of the accumulation of oxidative damage throughout the lifespan. Harman further refined his theory in 1972, highlighting the role of mitochondria as not only the primary cellular sources of ROS but also their primary target. Accordingly, interventions that mitigate oxidative stress, particularly at the mitochondrial level, have the potential to slow aging and delay the onset of age-related pathology, thus extending healthspan, i.e., the number of years for which a person is healthy and free of disease. However, there is also compelling evidence that oxidative stress does not necessarily predict lifespan or the clinical outcomes of age-associated pathologies, denoting the importance of the critical assessment of the pros and cons of antioxidant therapies as anti-aging interventions.

We invite you to contribute original research as well as review articles to this Special Issue aimed at critically examining the potential of pharmacological and non-pharmacological antioxidant therapies in aging and age-related diseases at the molecular, cellular, biochemical, and physiological levels, as well as clinical, pre-clinical, and translational research in the field of anti-aging antioxidant therapies.

Keywords

  • Aging
  • Oxidative stress
  • Lifespan
  • Model organisms
  • Neurodegeneration
  • Antioxidants
  • Lifestyle
  • oxida

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Published Papers (8 papers)

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Research

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10 pages, 1851 KiB  
Article
Human Placental Extract Delays In Vitro Cellular Senescence through the Activation of NRF2-Mediated Antioxidant Pathway
by Liguo Huang, Lit-Chein Chin, Koichi Kimura and Yasukazu Nakahata
Antioxidants 2022, 11(8), 1545; https://doi.org/10.3390/antiox11081545 - 10 Aug 2022
Cited by 5 | Viewed by 2792
Abstract
Senescent cells accumulate in the organs of aged animals and exacerbate organ dysfunction, resulting in age-related diseases. Oxidative stress accelerates cellular senescence. Placental extract, used in the alleviation of menopausal symptoms and promotion of wound healing and liver regeneration, reportedly protects against oxidative [...] Read more.
Senescent cells accumulate in the organs of aged animals and exacerbate organ dysfunction, resulting in age-related diseases. Oxidative stress accelerates cellular senescence. Placental extract, used in the alleviation of menopausal symptoms and promotion of wound healing and liver regeneration, reportedly protects against oxidative stress. In this study, we investigated the effects of human placental extract (HPE) on cellular senescence in normal human dermal fibroblasts (NHDFs) under oxidative stress conditions. We demonstrated that HPE delays the onset of cellular senescence. Next-generation sequencing analysis revealed that under oxidative stress conditions, HPE treatment enhanced the expression of the antioxidant genes CYGB, APOE, NQO1, and PTGS1. Further, HPE treatment under oxidative stress conditions increased the protein level of nuclear factor-erythroid factor 2-related factor 2 (NRF2)—a vital molecule in the antioxidant pathway—via post-transcriptional and/or post-translational regulations. These findings indicate that HPE treatment in NHDFs, under chronic oxidative stress, delays cellular senescence by mitigating oxidative stress via upregulation of the NRF2-mediated antioxidant pathway, and HPE treatment could potentially ameliorate skin-aging-associated damage, in vivo. Full article
(This article belongs to the Special Issue ROS in Aging and Age-Related Disease)
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11 pages, 466 KiB  
Article
(−)-Epicatechin-Enriched Extract from Camellia sinensis Improves Regulation of Muscle Mass and Function: Results from a Randomized Controlled Trial
by Hyeyeong Seo, Seok-Hee Lee, Yooheon Park, Hee-Seok Lee, Jeong Sup Hong, Cho Young Lim, Dong Hyeon Kim, Sung-Soo Park, Hyung Joo Suh and Ki-Bae Hong
Antioxidants 2021, 10(7), 1026; https://doi.org/10.3390/antiox10071026 - 25 Jun 2021
Cited by 11 | Viewed by 5505
Abstract
Loss of skeletal muscle mass and function with age represents an important source of frailty and functional decline in the elderly. Antioxidants from botanical extracts have been shown to enhance the development, mass, and strength of skeletal muscle by influencing age-related cellular and [...] Read more.
Loss of skeletal muscle mass and function with age represents an important source of frailty and functional decline in the elderly. Antioxidants from botanical extracts have been shown to enhance the development, mass, and strength of skeletal muscle by influencing age-related cellular and molecular processes. Tannase-treated green tea extract contains high levels of the antioxidants (−)-epicatechin (EC) and gallic acid that may have therapeutic benefits for age-related muscle decline. The aim of this study was to investigate the effect of tannase-treated green tea extract on various muscle-related parameters, without concomitant exercise, in a single-center, randomized, double-blind, placebo-controlled study. Administration of tannase-treated green tea extract (600 mg/day) for 12 weeks significantly increased isokinetic flexor muscle and handgrip strength in the treatment group compared with those in the placebo (control) group. In addition, the control group showed a significant decrease in arm muscle mass after 12 weeks, whereas no significant change was observed in the treatment group. Blood serum levels of follistatin, myostatin, high-sensitivity C-reactive protein (hs-CRP), interleukin (IL)-6, IL-8, insulin-like growth factor-1 (IGF-1), and cortisol were analyzed, and the decrease in myostatin resulting from the administration of tannase-treated green tea extract was found to be related to the change in muscle mass and strength. In summary, oral administration of tannase-treated green tea extract containing antioxidants without concomitant exercise can improve muscle mass and strength and may have therapeutic benefits in age-related muscle function decline. Full article
(This article belongs to the Special Issue ROS in Aging and Age-Related Disease)
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11 pages, 1599 KiB  
Article
Calcium Dobesilate Reverses Cognitive Deficits and Anxiety-Like Behaviors in the D-Galactose-Induced Aging Mouse Model through Modulation of Oxidative Stress
by Elham Hakimizadeh, Mohammad Zamanian, Lydia Giménez-Llort, Clara Sciorati, Marjan Nikbakhtzadeh, Małgorzata Kujawska, Ayat Kaeidi, Jalal Hassanshahi and Iman Fatemi
Antioxidants 2021, 10(5), 649; https://doi.org/10.3390/antiox10050649 - 23 Apr 2021
Cited by 14 | Viewed by 4983
Abstract
The long-term treatment of mice with D-galactose (D-gal) induces the overproduction of reactive oxygen species (ROS) and is a well-accepted experimental model of oxidative stress-linked cognitive disorders in physiological aging. Calcium dobesilate (CaD, Doxium®) is an established vasoactive and angioprotective drug [...] Read more.
The long-term treatment of mice with D-galactose (D-gal) induces the overproduction of reactive oxygen species (ROS) and is a well-accepted experimental model of oxidative stress-linked cognitive disorders in physiological aging. Calcium dobesilate (CaD, Doxium®) is an established vasoactive and angioprotective drug commonly used for the clinical treatment of diabetic retinopathy and chronic venous insufficiency. It has antioxidant properties and controls vascular permeability. In the current study, we evaluated the protective effects of CaD (50 and 100 mg/kg/day p.o.) in male mice treated with D-gal (500 mg/kg/day p.o.) for six weeks. Results demonstrated that body weight loss, anxiety-like and cognitive impairments of D-gal-treated animals were reversed by CaD administration as evaluated by the measurement of mice performance in elevated plus-maze, Y-maze, and shuttle box tests. CaD treatment also inhibited the oxidative stress in aging mouse brains by decreasing malondialdehyde (MDA) levels and increasing superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) enzyme activities. These results could open new perspectives for the clinical use of CaD in treating and preventing cognitive impairment in older people. Full article
(This article belongs to the Special Issue ROS in Aging and Age-Related Disease)
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Review

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21 pages, 1147 KiB  
Review
Protective Role of Mitochondrial Uncoupling Proteins against Age-Related Oxidative Stress in Type 2 Diabetes Mellitus
by Maša Čater and Lidija Križančić Bombek
Antioxidants 2022, 11(8), 1473; https://doi.org/10.3390/antiox11081473 - 28 Jul 2022
Cited by 24 | Viewed by 4682
Abstract
The accumulation of oxidative damage to DNA and other biomolecules plays an important role in the etiology of aging and age-related diseases such as type 2 diabetes mellitus (T2D), atherosclerosis, and neurodegenerative disorders. Mitochondrial DNA (mtDNA) is especially sensitive to oxidative stress. Mitochondrial [...] Read more.
The accumulation of oxidative damage to DNA and other biomolecules plays an important role in the etiology of aging and age-related diseases such as type 2 diabetes mellitus (T2D), atherosclerosis, and neurodegenerative disorders. Mitochondrial DNA (mtDNA) is especially sensitive to oxidative stress. Mitochondrial dysfunction resulting from the accumulation of mtDNA damage impairs normal cellular function and leads to a bioenergetic crisis that accelerates aging and associated diseases. Age-related mitochondrial dysfunction decreases ATP production, which directly affects insulin secretion by pancreatic beta cells and triggers the gradual development of the chronic metabolic dysfunction that characterizes T2D. At the same time, decreased glucose oxidation in skeletal muscle due to mitochondrial damage leads to prolonged postprandial blood glucose rise, which further worsens glucose homeostasis. ROS are not only highly reactive by-products of mitochondrial respiration capable of oxidizing DNA, proteins, and lipids but can also function as signaling and effector molecules in cell membranes mediating signal transduction and inflammation. Mitochondrial uncoupling proteins (UCPs) located in the inner mitochondrial membrane of various tissues can be activated by ROS to protect cells from mitochondrial damage. Mitochondrial UCPs facilitate the reflux of protons from the mitochondrial intermembrane space into the matrix, thereby dissipating the proton gradient required for oxidative phosphorylation. There are five known isoforms (UCP1-UCP5) of mitochondrial UCPs. UCP1 can indirectly reduce ROS formation by increasing glutathione levels, thermogenesis, and energy expenditure. In contrast, UCP2 and UCP3 regulate fatty acid metabolism and insulin secretion by beta cells and modulate insulin sensitivity. Understanding the functions of UCPs may play a critical role in developing pharmacological strategies to combat T2D. This review summarizes the current knowledge on the protective role of various UCP homologs against age-related oxidative stress in T2D. Full article
(This article belongs to the Special Issue ROS in Aging and Age-Related Disease)
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33 pages, 2904 KiB  
Review
Focus on the Contribution of Oxidative Stress in Skin Aging
by Federica Papaccio, Andrea D′Arino, Silvia Caputo and Barbara Bellei
Antioxidants 2022, 11(6), 1121; https://doi.org/10.3390/antiox11061121 - 6 Jun 2022
Cited by 107 | Viewed by 12451
Abstract
Skin aging is one of the most evident signs of human aging. Modification of the skin during the life span is characterized by fine lines and wrinkling, loss of elasticity and volume, laxity, rough-textured appearance, and pallor. In contrast, photoaged skin is associated [...] Read more.
Skin aging is one of the most evident signs of human aging. Modification of the skin during the life span is characterized by fine lines and wrinkling, loss of elasticity and volume, laxity, rough-textured appearance, and pallor. In contrast, photoaged skin is associated with uneven pigmentation (age spot) and is markedly wrinkled. At the cellular and molecular level, it consists of multiple interconnected processes based on biochemical reactions, genetic programs, and occurrence of external stimulation. The principal cellular perturbation in the skin driving senescence is the alteration of oxidative balance. In chronological aging, reactive oxygen species (ROS) are produced mainly through cellular oxidative metabolism during adenosine triphosphate (ATP) generation from glucose and mitochondrial dysfunction, whereas in extrinsic aging, loss of redox equilibrium is caused by environmental factors, such as ultraviolet radiation, pollution, cigarette smoking, and inadequate nutrition. During the aging process, oxidative stress is attributed to both augmented ROS production and reduced levels of enzymatic and non-enzymatic protectors. Apart from the evident appearance of structural change, throughout aging, the skin gradually loses its natural functional characteristics and regenerative potential. With aging, the skin immune system also undergoes functional senescence manifested as a reduced ability to counteract infections and augmented frequency of autoimmune and neoplastic diseases. This review proposes an update on the role of oxidative stress in the appearance of the clinical manifestation of skin aging, as well as of the molecular mechanisms that underline this natural phenomenon sometimes accelerated by external factors. Full article
(This article belongs to the Special Issue ROS in Aging and Age-Related Disease)
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28 pages, 3408 KiB  
Review
Molecular Mechanisms and Therapeutic Potential of α- and β-Asarone in the Treatment of Neurological Disorders
by Rengasamy Balakrishnan, Duk-Yeon Cho, In-Su Kim, Sang-Ho Seol and Dong-Kug Choi
Antioxidants 2022, 11(2), 281; https://doi.org/10.3390/antiox11020281 - 29 Jan 2022
Cited by 32 | Viewed by 5748
Abstract
Neurological disorders are important causes of morbidity and mortality around the world. The increasing prevalence of neurological disorders, associated with an aging population, has intensified the societal burden associated with these diseases, for which no effective treatment strategies currently exist. Therefore, the identification [...] Read more.
Neurological disorders are important causes of morbidity and mortality around the world. The increasing prevalence of neurological disorders, associated with an aging population, has intensified the societal burden associated with these diseases, for which no effective treatment strategies currently exist. Therefore, the identification and development of novel therapeutic approaches, able to halt or reverse neuronal loss by targeting the underlying causal factors that lead to neurodegeneration and neuronal cell death, are urgently necessary. Plants and other natural products have been explored as sources of safe, naturally occurring secondary metabolites with potential neuroprotective properties. The secondary metabolites α- and β-asarone can be found in high levels in the rhizomes of the medicinal plant Acorus calamus (L.). α- and β-asarone exhibit multiple pharmacological properties including antioxidant, anti-inflammatory, antiapoptotic, anticancer, and neuroprotective effects. This paper aims to provide an overview of the current research on the therapeutic potential of α- and β-asarone in the treatment of neurological disorders, particularly neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), as well as cerebral ischemic disease, and epilepsy. Current research indicates that α- and β-asarone exert neuroprotective effects by mitigating oxidative stress, abnormal protein accumulation, neuroinflammation, neurotrophic factor deficit, and promoting neuronal cell survival, as well as activating various neuroprotective signalling pathways. Although the beneficial effects exerted by α- and β-asarone have been demonstrated through in vitro and in vivo animal studies, additional research is required to translate laboratory results into safe and effective therapies for patients with AD, PD, and other neurological and neurodegenerative diseases. Full article
(This article belongs to the Special Issue ROS in Aging and Age-Related Disease)
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25 pages, 11769 KiB  
Review
Peroxisomal Stress Response and Inter-Organelle Communication in Cellular Homeostasis and Aging
by Jinoh Kim and Hua Bai
Antioxidants 2022, 11(2), 192; https://doi.org/10.3390/antiox11020192 - 19 Jan 2022
Cited by 29 | Viewed by 10126
Abstract
Peroxisomes are key regulators of cellular and metabolic homeostasis. These organelles play important roles in redox metabolism, the oxidation of very-long-chain fatty acids (VLCFAs), and the biosynthesis of ether phospholipids. Given the essential role of peroxisomes in cellular homeostasis, peroxisomal dysfunction has been [...] Read more.
Peroxisomes are key regulators of cellular and metabolic homeostasis. These organelles play important roles in redox metabolism, the oxidation of very-long-chain fatty acids (VLCFAs), and the biosynthesis of ether phospholipids. Given the essential role of peroxisomes in cellular homeostasis, peroxisomal dysfunction has been linked to various pathological conditions, tissue functional decline, and aging. In the past few decades, a variety of cellular signaling and metabolic changes have been reported to be associated with defective peroxisomes, suggesting that many cellular processes and functions depend on peroxisomes. Peroxisomes communicate with other subcellular organelles, such as the nucleus, mitochondria, endoplasmic reticulum (ER), and lysosomes. These inter-organelle communications are highly linked to the key mechanisms by which cells surveil defective peroxisomes and mount adaptive responses to protect them from damages. In this review, we highlight the major cellular changes that accompany peroxisomal dysfunction and peroxisomal inter-organelle communication through membrane contact sites, metabolic signaling, and retrograde signaling. We also discuss the age-related decline of peroxisomal protein import and its role in animal aging and age-related diseases. Unlike other organelle stress response pathways, such as the unfolded protein response (UPR) in the ER and mitochondria, the cellular signaling pathways that mediate stress responses to malfunctioning peroxisomes have not been systematically studied and investigated. Here, we coin these signaling pathways as “peroxisomal stress response pathways”. Understanding peroxisomal stress response pathways and how peroxisomes communicate with other organelles are important and emerging areas of peroxisome research. Full article
(This article belongs to the Special Issue ROS in Aging and Age-Related Disease)
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43 pages, 2495 KiB  
Review
Acetyl-CoA Metabolism and Histone Acetylation in the Regulation of Aging and Lifespan
by Patrick C. Bradshaw
Antioxidants 2021, 10(4), 572; https://doi.org/10.3390/antiox10040572 - 8 Apr 2021
Cited by 83 | Viewed by 16242
Abstract
Acetyl-CoA is a metabolite at the crossroads of central metabolism and the substrate of histone acetyltransferases regulating gene expression. In many tissues fasting or lifespan extending calorie restriction (CR) decreases glucose-derived metabolic flux through ATP-citrate lyase (ACLY) to reduce cytoplasmic acetyl-CoA levels to [...] Read more.
Acetyl-CoA is a metabolite at the crossroads of central metabolism and the substrate of histone acetyltransferases regulating gene expression. In many tissues fasting or lifespan extending calorie restriction (CR) decreases glucose-derived metabolic flux through ATP-citrate lyase (ACLY) to reduce cytoplasmic acetyl-CoA levels to decrease activity of the p300 histone acetyltransferase (HAT) stimulating pro-longevity autophagy. Because of this, compounds that decrease cytoplasmic acetyl-CoA have been described as CR mimetics. But few authors have highlighted the potential longevity promoting roles of nuclear acetyl-CoA. For example, increasing nuclear acetyl-CoA levels increases histone acetylation and administration of class I histone deacetylase (HDAC) inhibitors increases longevity through increased histone acetylation. Therefore, increased nuclear acetyl-CoA likely plays an important role in promoting longevity. Although cytoplasmic acetyl-CoA synthetase 2 (ACSS2) promotes aging by decreasing autophagy in some peripheral tissues, increased glial AMPK activity or neuronal differentiation can stimulate ACSS2 nuclear translocation and chromatin association. ACSS2 nuclear translocation can result in increased activity of CREB binding protein (CBP), p300/CBP-associated factor (PCAF), and other HATs to increase histone acetylation on the promoter of neuroprotective genes including transcription factor EB (TFEB) target genes resulting in increased lysosomal biogenesis and autophagy. Much of what is known regarding acetyl-CoA metabolism and aging has come from pioneering studies with yeast, fruit flies, and nematodes. These studies have identified evolutionary conserved roles for histone acetylation in promoting longevity. Future studies should focus on the role of nuclear acetyl-CoA and histone acetylation in the control of hypothalamic inflammation, an important driver of organismal aging. Full article
(This article belongs to the Special Issue ROS in Aging and Age-Related Disease)
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