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Journal articles on the topic 'Adipose tissue, senescence, aging, oxidative stress'

Author: Grafiati

Published: 11 March 2023

Last updated: 31 July 2025

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1

Gorwood, Jennifer, Tina Ejlalmanesh, Christine Bourgeois, et al. "SIV Infection and the HIV Proteins Tat and Nef Induce Senescence in Adipose Tissue and Human Adipose Stem Cells, Resulting in Adipocyte Dysfunction." Cells 9, no. 4 (2020): 854. http://dx.doi.org/10.3390/cells9040854.

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Background: Aging is characterized by adipose tissue senescence, inflammation, and fibrosis, with trunk fat accumulation. Aging HIV-infected patients have a higher risk of trunk fat accumulation than uninfected individuals—suggesting that viral infection has a role in adipose tissue aging. We previously demonstrated that HIV/SIV infection and the Tat and Nef viral proteins were responsible for adipose tissue fibrosis and impaired adipogenesis. We hypothesized that SIV/HIV infection and viral proteins could induce adipose tissue senescence and thus lead to adipocyte dysfunctions. Methods: Featu

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Balasubramanian, Priya, Tamas Kiss, Rafal Gulej, et al. "Accelerated Aging Induced by an Unhealthy High-Fat Diet: Initial Evidence for the Role of Nrf2 Deficiency and Impaired Stress Resilience in Cellular Senescence." Nutrients 16, no. 7 (2024): 952. http://dx.doi.org/10.3390/nu16070952.

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High-fat diets (HFDs) have pervaded modern dietary habits, characterized by their excessive saturated fat content and low nutritional value. Epidemiological studies have compellingly linked HFD consumption to obesity and the development of type 2 diabetes mellitus. Moreover, the synergistic interplay of HFD, obesity, and diabetes expedites the aging process and prematurely fosters age-related diseases. However, the underlying mechanisms driving these associations remain enigmatic. One of the most conspicuous hallmarks of aging is the accumulation of highly inflammatory senescent cells, with mo

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Schosserer, Markus, Johannes Grillari, Christian Wolfrum, and Marcel Scheideler. "Age-Induced Changes in White, Brite, and Brown Adipose Depots: A Mini-Review." Gerontology 64, no. 3 (2017): 229–36. http://dx.doi.org/10.1159/000485183.

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Aging is a time-related process of functional decline at organelle, cellular, tissue, and organismal level that ultimately limits life. Cellular senescence is a state of permanent growth arrest in response to stress and one of the major drivers of aging and age-related disorders. Senescent cells accumulate with age, and removal of these cells delays age-related disorders in different tissues and prolongs healthy lifespan. One of the most studied aging mechanisms is the accumulation of reactive oxygen species damage in cells, organs, and organisms over time. Elevated oxidative stress is also fo

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Caron, Martine, Martine Auclair, Anais Vissian, Corinne Vigouroux, and Jacqueline Capeau. "Contribution of Mitochondrial Dysfunction and Oxidative Stress to Cellular Premature Senescence Induced by Antiretroviral Thymidine Analogues." Antiviral Therapy 13, no. 1 (2008): 27–38. http://dx.doi.org/10.1177/135965350801300103.

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Objectives Treatment of HIV-infected patients is associated with early onset of aging-related comorbidities. Some of the adverse effects of antiretroviral therapy have been attributed to the mitochondrial toxicity of nucleoside reverse transcriptase inhibitors (NRTI), and it is of note that mitochondrial dysfunction and oxidative stress are involved in the aging processes. In this regard, we examined whether NRTIs could accelerate the senescence of cultured cells. Methods Human fibroblasts were exposed to NRTIs from culture passage 1 to 14. Cytochrome c-oxidase (COX) subunits 2 and 4, mitochon

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Nandini Mode and Chaitanya B. "Senescence-Associated Secretory Phenotype (SASP) in Diabetes." Journal of Pharma Insights and Research 3, no. 1 (2025): 205–11. https://doi.org/10.69613/qjzz6g14.

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Cellular senescence represents a critical biological process characterized by permanent cell cycle arrest and distinct metabolic alterations. The senescence-associated secretory phenotype (SASP) has emerged as a fundamental mediator linking cellular aging to various pathological conditions, including diabetes mellitus. Recent investigations have unveiled the intricate relationship between SASP and pancreatic β-cell dysfunction, insulin resistance, and diabetic complications. The accumulation of senescent cells in pancreatic islets correlates with diminished insulin production and secretion, wh

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Russo, Lara, Serena Babboni, Maria Grazia Andreassi, et al. "Treating Metabolic Dysregulation and Senescence by Caloric Restriction: Killing Two Birds with One Stone?" Antioxidants 14, no. 1 (2025): 99. https://doi.org/10.3390/antiox14010099.

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Cellular senescence is a state of permanent cell cycle arrest accompanied by metabolic activity and characteristic phenotypic changes. This process is crucial for developing age-related diseases, where excessive calorie intake accelerates metabolic dysfunction and aging. Overnutrition disturbs key metabolic pathways, including insulin/insulin-like growth factor signaling (IIS), the mammalian target of rapamycin (mTOR), and AMP-activated protein kinase. The dysregulation of these pathways contributes to insulin resistance, impaired autophagy, exacerbated oxidative stress, and mitochondrial dysf

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Kornicka, K., R. Walczak, A. Mucha, and K. Marycz. "Released from ZrO2/SiO2 coating resveratrol inhibits senescence and oxidative stress of human adipose-derived stem cells (ASC)." Open Chemistry 16, no. 1 (2018): 481–95. http://dx.doi.org/10.1515/chem-2018-0039.

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AbstractThe rapid aging of the population results in increased number of metabolic and degenerative disorders, especially in the elderly.Thus, a novel approach in the fields of orthopedic and reconstructive surgery for bone regeneration is strongly desirable. A new perspective in the therapy of bone fractures is tissue engineering which combines living cells with biomaterials to develop modern substitutes that can restore tissue functions. Metallic biomaterials, including stainless steel and pure titanium, have been extensively used for the fabrication of surgical implants over decades. Chemic

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Wang, Xiujuan, Rui Liu, Chan Wei, Meihong Xu, and Yong Li. "Exogenous Nucleotides Improved the Oxidative Stress and Sirt-1 Protein Level of Brown Adipose Tissue on Senescence-Accelerated Mouse Prone-8 (SAMP8) Mice." Nutrients 14, no. 14 (2022): 2796. http://dx.doi.org/10.3390/nu14142796.

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Brown adipose tissue (BAT) is of great importance in rodents for maintaining their core temperature via non-shivering thermogenesis in the mitochondria. BAT′s thermogenic function has been shown to decline with age. The activation of adenosine 5′-monophosphate (AMP)-activated protein kinase/sirtuin-1 (AMPK/Sirt-1) is effective in regulating mitochondrial function. Exogenous nucleotides (NTs) are regulatory factors in many biological processes. Nicotinamide mononucleotide (NMN), which is a derivative of NTs, is widely known as a Sirt-1 activator in liver and muscle, but the effect of NMN and NT

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Kornicka, Katarzyna, Krzysztof Marycz, Krzysztof Andrzej Tomaszewski, Monika Marędziak, and Agnieszka Śmieszek. "The Effect of Age on Osteogenic and Adipogenic Differentiation Potential of Human Adipose Derived Stromal Stem Cells (hASCs) and the Impact of Stress Factors in the Course of the Differentiation Process." Oxidative Medicine and Cellular Longevity 2015 (2015): 1–20. http://dx.doi.org/10.1155/2015/309169.

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Human adipose tissue is a great source of autologous mesenchymal stem cells (hASCs), which are recognized for their vast therapeutic applications. Their ability to self-renew and differentiate into several lineages makes them a promising tool for cell-based therapies in different types of degenerative diseases. Thus it is crucial to evaluate age-related changes in hASCs, as the elderly are a group that will benefit most from their considerable potential. In this study we investigated the effect of donor age on growth kinetics, cellular senescence marker levels, and osteogenic and adipogenic po

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Park, Jeong Seop, Jiyuan Piao, Gabee Park, and Hyun Sook Hong. "Substance-P Restores Cellular Activity of ADSC Impaired by Oxidative Stress." Antioxidants 9, no. 10 (2020): 978. http://dx.doi.org/10.3390/antiox9100978.

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Oxidative stress induces cellular damage, which accelerates aging and promotes the development of serious illnesses. Adipose-derived stem cells (ADSCs) are novel cellular therapeutic tools and have been applied for tissue regeneration. However, ADSCs from aged and diseased individuals may be affected in vivo by the accumulation of free radicals, which can impair their therapeutic efficacy. Substance-P (SP) is a neuropeptide that is known to rescue stem cells from senescence and inflammatory attack, and this study explored the restorative effect of SP on ADSCs under oxidative stress. ADSCs were

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Lefranc, Clara, Malou Friederich-Persson, Fabienne Foufelle, Aurélie Nguyen Dinh Cat, and Frédéric Jaisser. "Adipocyte-Mineralocorticoid Receptor Alters Mitochondrial Quality Control Leading to Mitochondrial Dysfunction and Senescence of Visceral Adipose Tissue." International Journal of Molecular Sciences 22, no. 6 (2021): 2881. http://dx.doi.org/10.3390/ijms22062881.

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Mineralocorticoid receptor (MR) expression is increased in the adipose tissue (AT) of obese patients and animals. We previously demonstrated that adipocyte-MR overexpression in mice (Adipo-MROE mice) is associated with metabolic alterations. Moreover, we showed that MR regulates mitochondrial dysfunction and cellular senescence in the visceral AT of obese db/db mice. Our hypothesis is that adipocyte-MR overactivation triggers mitochondrial dysfunction and cellular senescence, through increased mitochondrial oxidative stress (OS). Using the Adipo-MROE mice with conditional adipocyte-MR expressi

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Valverde, Mahara, та Aarón Sánchez-Brito. "Sustained Activation of TNFα-Induced DNA Damage Response in Newly Differentiated Adipocytes". International Journal of Molecular Sciences 22, № 19 (2021): 10548. http://dx.doi.org/10.3390/ijms221910548.

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The response to DNA damage is the mechanism that allows the interaction between stress signals, inflammatory secretions, DNA repair, and maintenance of cell and tissue homeostasis. Adipocyte dysfunction is the cellular trigger for various disease states such as insulin resistance, diabetes, and obesity, among many others. Previously, our group demonstrated that adipogenesis per se, from mesenchymal/stromal stem cells derived from human adipose tissue (hASCs), involves an accumulation of DNA damage and a gradual loss of the repair capacity of oxidative DNA damage. Therefore, our objective was t

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Liang, Yicong, Devesh Kaushal, and Robert Beaumont Wilson. "Cellular Senescence and Extracellular Vesicles in the Pathogenesis and Treatment of Obesity—A Narrative Review." International Journal of Molecular Sciences 25, no. 14 (2024): 7943. http://dx.doi.org/10.3390/ijms25147943.

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This narrative review explores the pathophysiology of obesity, cellular senescence, and exosome release. When exposed to excessive nutrients, adipocytes develop mitochondrial dysfunction and generate reactive oxygen species with DNA damage. This triggers adipocyte hypertrophy and hypoxia, inhibition of adiponectin secretion and adipogenesis, increased endoplasmic reticulum stress and maladaptive unfolded protein response, metaflammation, and polarization of macrophages. Such feed-forward cycles are not resolved by antioxidant systems, heat shock response pathways, or DNA repair mechanisms, res

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Marycz, Krzysztof, Katarzyna Kornicka, Katarzyna Basinska, and Aleksandra Czyrek. "Equine Metabolic Syndrome Affects Viability, Senescence, and Stress Factors of Equine Adipose-Derived Mesenchymal Stromal Stem Cells: New Insight into EqASCs Isolated from EMS Horses in the Context of Their Aging." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–17. http://dx.doi.org/10.1155/2016/4710326.

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Currently, equine metabolic syndrome (EMS), an endocrine disease linked to insulin resistance, affects an increasing number of horses. However, little is known about the effect of EMS on mesenchymal stem cells that reside in adipose tissue (ASC). Thus it is crucial to evaluate the viability and growth kinetics of these cells, particularly in terms of their application in regenerative medicine. In this study, we investigated the proliferative capacity, morphological features, and accumulation of oxidative stress factors in mesenchymal stem cells isolated from healthy animals (ASCN) and horses s

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Kim, Yu-Hee, Kyung-Ah Cho, Minhwa Park, So-Youn Woo, and Kyung-Ha Ryu. "Conditioned medium from tonsil-derived mesenchymal stem cells promotes adiponectin production." Journal of Immunology 198, no. 1_Supplement (2017): 206.21. http://dx.doi.org/10.4049/jimmunol.198.supp.206.21.

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Abstract Mesenchymal stem cells (MSCs) and conditioned medium (MSC CM) are now considered to be a good source for the development of regenerative medicine. Previously, we reported that tonsil-derived MSC (T-MSC) CM produces visceral fat reducing effects. As reduction in visceral adiposity is closely related to the increase of adiponectin in circulation, we sought to extend our previous findings and explore the effects of T-MSC CM on adiponectin production. T-MSC CM was collected from previously isolated and characterized T-MSCs and injected into a senescence-accelerated mouse prone 6 (SAMP6),

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Zhou, C., Y. Q. Chen, Y. H. Zhu, et al. "Antiadipogenesis and Osseointegration of Strontium-Doped Implant Surfaces." Journal of Dental Research 98, no. 7 (2019): 795–802. http://dx.doi.org/10.1177/0022034519850574.

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The decreased bone density and increased marrow adiposity that occur with aging may influence the outcome of dental implants. Strontium (Sr), an anabolic agent for the treatment of osteoporosis, has an inhibitory effect on adipogenesis but favors osteogenesis of bone marrow–derived mesenchymal stem cells (BMSCs). However, little is known about the effects and mechanisms of local Sr release on adipogenesis during bone formation in aged bone. In this study, a potential dental implant material, Sr-doped titanium, was developed via a sandblasted, large-grit, and acid-etched (SLA) method combined w

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Pangrazzi, Luca, Erin Naismith, Carina Miggitsch, et al. "The impact of body mass index on adaptive immune cells in the human bone marrow." Immunity & Ageing 17, no. 1 (2020): 15. https://doi.org/10.1186/s12979-020-00186-w.

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<strong>Background: </strong>Obesity has been associated with chronic inflammation and oxidative stress. Both conditions play a determinant role in the pathogenesis of age-related diseases, such as immunosenescence. Adipose tissue can modulate the function of the immune system with the secretion of molecules influencing the phenotype of immune cells. The importance of the bone marrow (BM) in the maintenance of antigen-experienced adaptive immune cells has been documented in mice. Recently, some groups have investigated the survival of effector/memory T cells in the human BM. Despite this, whet

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de Lange, Pieter, Assunta Lombardi, Elena Silvestri, et al. "Physiological Approaches Targeting Cellular and Mitochondrial Pathways Underlying Adipose Organ Senescence." International Journal of Molecular Sciences 24, no. 14 (2023): 11676. http://dx.doi.org/10.3390/ijms241411676.

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The adipose organ is involved in many metabolic functions, ranging from the production of endocrine factors to the regulation of thermogenic processes. Aging is a natural process that affects the physiology of the adipose organ, leading to metabolic disorders, thus strongly impacting healthy aging. Cellular senescence modifies many functional aspects of adipose tissue, leading to metabolic alterations through defective adipogenesis, inflammation, and aberrant adipocytokine production, and in turn, it triggers systemic inflammation and senescence, as well as insulin resistance in metabolically

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Bu, Huaije, Sophia Wedel, Maria Cavinato, and Pidder Jansen-Dürr. "MicroRNA Regulation of Oxidative Stress-Induced Cellular Senescence." Oxidative Medicine and Cellular Longevity 2017 (2017): 1–12. http://dx.doi.org/10.1155/2017/2398696.

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Aging is a time-related process of functional deterioration at cellular, tissue, organelle, and organismal level that ultimately brings life to end. Cellular senescence, a state of permanent cell growth arrest in response to cellular stress, is believed to be the driver of the aging process and age-related disorders. The free radical theory of aging, referred to as oxidative stress (OS) theory below, is one of the most studied aging promoting mechanisms. In addition, genetics and epigenetics also play large roles in accelerating and/or delaying the onset of aging and aging-related diseases. Am

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Sharebiani, Hiva, Shayan Keramat, Abdolali Chavoshan, Bahar Fazeli, and Agata Stanek. "The Influence of Antioxidants on Oxidative Stress-Induced Vascular Aging in Obesity." Antioxidants 12, no. 6 (2023): 1295. http://dx.doi.org/10.3390/antiox12061295.

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Obesity is a worldwide trend that is growing in incidence very fast. Adipose tissue dysfunction caused by obesity is associated with the generation of oxidative stress. Obesity-induced oxidative stress and inflammation play a key role in the pathogenesis of vascular diseases. Vascular aging is one of the main pathogenesis mechanisms. The aim of this study is to review the effect of antioxidants on vascular aging caused by oxidative stress in obesity. In order to achieve this aim, this paper is designed to review obesity-caused adipose tissue remodeling, vascular aging generated by high levels

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Qin, Ying, Haoxin Liu, and Hongli Wu. "Cellular Senescence in Health, Disease, and Lens Aging." Pharmaceuticals 18, no. 2 (2025): 244. https://doi.org/10.3390/ph18020244.

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Background: Cellular senescence is a state of irreversible cell cycle arrest that serves as a critical regulator of tissue homeostasis, aging, and disease. While transient senescence contributes to development, wound healing, and tumor suppression, chronic senescence drives inflammation, tissue dysfunction, and age-related pathologies, including cataracts. Lens epithelial cells (LECs), essential for maintaining lens transparency, are particularly vulnerable to oxidative stress-induced senescence, which accelerates lens aging and cataract formation. This review examines the dual role of senesce

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Zhang, Le, Philip J. Ebenezer, Kalavathi Dasuri, et al. "Aging is associated with hypoxia and oxidative stress in adipose tissue: implications for adipose function." American Journal of Physiology-Endocrinology and Metabolism 301, no. 4 (2011): E599—E607. http://dx.doi.org/10.1152/ajpendo.00059.2011.

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As a part of aging there are known to be numerous alterations which occur in multiple tissues of the body, and the focus of this study was to determine the extent to which oxidative stress and hypoxia occur during adipose tissue aging. In our studies we demonstrate for the first time that aging is associated with both hypoxia (38% reduction in oxygen levels, Po2 21.7 mmHg) and increases reactive oxygen species in visceral fat depots of aging male C57Bl/6 mice. Interestingly, aging visceral fat depots were observed to have significantly less change in the expression of genes involved in redox r

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Ratushnyy, A. Yu. "OXIDATIVE STRESS AS SENECCENCE INDUCTOR FOR ADIPOSE-DERIVED MESENCHYMAL STROMAL CELLS." Aerospace and Environmental Medicine 57, no. 4 (2023): 58–63. http://dx.doi.org/10.21687/0233-528x-2023-57-4-58-63.

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Studies of tissue-specific mesenchymal stromal cells (MSCs) for medical purposes are inspired by their potential to multilineage differentiation, a broad spectrum of bioactive molecule secretion and other properties. Cell senescence induced by oxidative stress can alter the MSCs morphofunctional characteristics. The work was aimed at studying the senescence-related morphofunctional changes in adipose-derived MSCs (AD-MSCs) under sublethal oxidative stress. Viability of cells in 96 hours after adding 500 µМ H2O2 made up less than 5 % (incubation time – 6 hrs.). Percentage of survived cells in o

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Nandita H, Manohar M, and Gowda DV. "Recent Review on Oxidative stress, Cellular senescence and Age-Associated Diseases." International Journal of Research in Pharmaceutical Sciences 11, no. 2 (2020): 1331–42. http://dx.doi.org/10.26452/ijrps.v11i2.1990.

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Reactive Oxygen Species (ROS) is considered as the main factor of the Free Radical theory of aging over centuries and it indicates the pathophysiology of aging in mammals. ROS causes oxidative stress, which is a major component in the aging process of higher organisms. ROS also leads to many age-related diseases such as cancer, cardiovascular disease, diabetes, etc. ROS causes damage to most of the biological membranes that cause these chronic diseases. Enhanced ROS levels at the cellular level lead to cellular senescence. It is a stage of cells where growth arrest happens associated with the

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Woldhuis, Roy R., Maaike de Vries, Wim Timens, et al. "Link between increased cellular senescence and extracellular matrix changes in COPD." American Journal of Physiology-Lung Cellular and Molecular Physiology 319, no. 1 (2020): L48—L60. http://dx.doi.org/10.1152/ajplung.00028.2020.

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Chronic obstructive pulmonary disease (COPD) is associated with features of accelerated aging, including cellular senescence, DNA damage, oxidative stress, and extracellular matrix (ECM) changes. We propose that these features are particularly apparent in patients with severe, early-onset (SEO)-COPD. Whether fibroblasts from COPD patients display features of accelerated aging and whether this is also present in relatively young SEO-COPD patients is unknown. Therefore, we aimed to determine markers of aging in (SEO)-COPD-derived lung fibroblasts and investigate the impact on ECM. Aging hallmark

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Kornicka, K., D. Nawrocka, A. Lis-Bartos, M. Marędziak, and K. Marycz. "Polyurethane–polylactide-based material doped with resveratrol decreases senescence and oxidative stress of adipose-derived mesenchymal stromal stem cell (ASCs)." RSC Advances 7, no. 39 (2017): 24070–84. http://dx.doi.org/10.1039/c7ra02334k.

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The aim of this study was to evaluate the influence of resveratrol (RES)-doped polyurethane (TPU)–polylactide (PLA) biomaterials on the senescence and oxidative stress factor of adipose-derived stem cells (ASCs) for tissue engineering.

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Jia, Dandan, Huijie Zhang, Tiemin Liu, and Ru Wang. "Exercise Alleviates Aging of Adipose Tissue through Adipokine Regulation." Metabolites 14, no. 3 (2024): 135. http://dx.doi.org/10.3390/metabo14030135.

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Adipose tissue undergoes changes with aging, leading to increased adiposity, inflammatory cell infiltration, reduced angiogenesis, heightened oxidative stress, and alterations in its metabolic function. Regular exercise has been recognized as a powerful intervention that can positively influence adipose tissue health and mitigate the effects of aging. However, the molecular mechanisms underlying the benefits of regular exercise on aging adipose tissue function remain poorly understood. Adipokines released through regular exercise play a potential role in mitigating adipose tissue aging, enhanc

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Gu, Ke, Xiao-Mei Feng, Shao-Qing Sun, Xing-Yao Hao, and Yong Wen. "Yes-associated protein-mediated melatonin regulates the function of periodontal ligament stem cells under oxidative stress conditions." World Journal of Stem Cells 16, no. 11 (2024): 926–43. http://dx.doi.org/10.4252/wjsc.v16.i11.926.

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BACKGROUND Human periodontal ligament stem cells (PDLSCs) regenerate oral tissue. In vitro expansion causes replicative senescence in stem cells. This causes intracellular reactive oxygen species (ROS) accumulation, which can impair stem cell function. Tissue engineering efficiency is reduced by exogenous ROS stimulation, which causes premature senescence under oxidative stress. Melatonin (MT), a powerful free radical scavenger, can delay PDLSCs senescence but may not maintain stemness under oxidative stress. This experiment examined the effects of hydrogen peroxide-induced oxidative stress on

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Mechchate, Hamza, Aicha El Allam, Nasreddine El Omari, et al. "Vegetables and Their Bioactive Compounds as Anti-Aging Drugs." Molecules 27, no. 7 (2022): 2316. http://dx.doi.org/10.3390/molecules27072316.

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Aging is a continuous process over time that is mainly related to natural alterations in mechanical–biological processes. This phenomenon is due to several factors, including the time and energy of biological processes. Aging can be attributed to biological factors such as oxidative stress, cell longevity, and stem cell senescence. Currently, aging is associated with several diseases, such as neurodegenerative diseases, cancer, and other diseases related to oxidative stress. In addition, certain natural molecules, including those derived from vegetables, have shown the ability to delay the agi

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Kobayashi, Hiroshi, Mai Umetani, Miki Nishio, Hiroshi Shigetomi, Shogo Imanaka, and Hiratsugu Hashimoto. "Molecular Mechanisms of Cellular Senescence in Age-Related Endometrial Dysfunction." Cells 14, no. 12 (2025): 858. https://doi.org/10.3390/cells14120858.

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The endometrium is essential for reproductive function, supporting implantation and pregnancy through mechanisms such as hormonal responsiveness, immune regulation, and tissue regeneration. Aging disrupts these processes, with cellular senescence—marked by irreversible cell cycle arrest due to DNA damage and oxidative stress—being a key contributor. While senescence aids in tumor suppression and tissue repair, its dysregulation impairs endometrial function. Central to this regulation are p53, AMPK, and mTOR, which coordinate stress responses, metabolic regulation, and proliferation control. p5

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Maharajan, Nagarajan, Chitra Devi Ganesan, Changjong Moon, Chul-Ho Jang, Won-Keun Oh, and Gwang-Won Cho. "Licochalcone D Ameliorates Oxidative Stress-Induced Senescence via AMPK Activation." International Journal of Molecular Sciences 22, no. 14 (2021): 7324. http://dx.doi.org/10.3390/ijms22147324.

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Increased oxidative stress is a crucial factor for the progression of cellular senescence and aging. The present study aimed to investigate the effects of licochalcone D (Lico D) on oxidative stress-induced senescence, both in vitro and in vivo, and explore its potential mechanisms. Hydrogen peroxide (200 µM for double time) and D-galactose (D-Gal) (150 mg/kg) were used to induce oxidative stress in human bone marrow-mesenchymal stem cells (hBM-MSCs) and mice, respectively. We performed the SA-β-gal assay and evaluated the senescence markers, activation of AMPK, and autophagy. Lico D potential

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Popa, Alina Delia, Otilia Niță, Lavinia Caba, et al. "From the Sun to the Cell: Examining Obesity through the Lens of Vitamin D and Inflammation." Metabolites 14, no. 1 (2023): 4. http://dx.doi.org/10.3390/metabo14010004.

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Obesity affects more than one billion people worldwide and often leads to cardiometabolic chronic comorbidities. It induces senescence-related alterations in adipose tissue, and senescence is closely linked to obesity. Fully elucidating the pathways through which vitamin D exerts anti-inflammatory effects may improve our understanding of local adipose tissue inflammation and the pathogenesis of metabolic disorders. In this narrative review, we compiled and analyzed the literature from diverse academic sources, focusing on recent developments to provide a comprehensive overview of the effect of

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Serino, Alexa, and Gloria Salazar. "Protective Role of Polyphenols against Vascular Inflammation, Aging and Cardiovascular Disease." Nutrients 11, no. 1 (2018): 53. http://dx.doi.org/10.3390/nu11010053.

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Aging is a major risk factor in the development of chronic diseases affecting various tissues including the cardiovascular system, muscle and bones. Age-related diseases are a consequence of the accumulation of cellular damage and reduced activity of protective stress response pathways leading to low-grade systemic inflammation and oxidative stress. Both inflammation and oxidative stress are major contributors to cellular senescence, a process in which cells stop proliferating and become dysfunctional by secreting inflammatory molecules, reactive oxygen species (ROS) and extracellular matrix c

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Salmon, Ellen E., Jason J. Breithaupt, and George A. Truskey. "Application of Oxidative Stress to a Tissue-Engineered Vascular Aging Model Induces Endothelial Cell Senescence and Activation." Cells 9, no. 5 (2020): 1292. http://dx.doi.org/10.3390/cells9051292.

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Clinical studies have established a connection between oxidative stress, aging, and atherogenesis. These factors contribute to senescence and inflammation in the endothelium and significant reductions in endothelium-dependent vasoreactivity in aged patients. Tissue-engineered blood vessels (TEBVs) recapitulate the structure and function of arteries and arterioles in vitro. We developed a TEBV model for vascular senescence and examined the relative influence of endothelial cell and smooth muscle cell senescence on vasoreactivity. Senescence was induced in 2D endothelial cell cultures and TEBVs

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Findeisen, Hannes M., Kevin J. Pearson, Florence Gizard, et al. "Oxidative Stress Accumulates in Adipose Tissue during Aging and Inhibits Adipogenesis." PLoS ONE 6, no. 4 (2011): e18532. http://dx.doi.org/10.1371/journal.pone.0018532.

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Varesi, Angelica, Salvatore Chirumbolo, Lucrezia Irene Maria Campagnoli, et al. "The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence." Antioxidants 11, no. 7 (2022): 1224. http://dx.doi.org/10.3390/antiox11071224.

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Cellular senescence is an irreversible state of cell cycle arrest occurring in response to stressful stimuli, such as telomere attrition, DNA damage, reactive oxygen species, and oncogenic proteins. Although beneficial and protective in several physiological processes, an excessive senescent cell burden has been involved in various pathological conditions including aging, tissue dysfunction and chronic diseases. Oxidative stress (OS) can drive senescence due to a loss of balance between pro-oxidant stimuli and antioxidant defences. Therefore, the identification and characterization of antioxid

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Shen, Chieh-Yu, Cheng-Hsun Lu, Cheng-Han Wu, et al. "Molecular Basis of Accelerated Aging with Immune Dysfunction-Mediated Inflammation (Inflamm-Aging) in Patients with Systemic Sclerosis." Cells 10, no. 12 (2021): 3402. http://dx.doi.org/10.3390/cells10123402.

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Systemic sclerosis (SSc) is a chronic connective tissue disorder characterized by immune dysregulation, chronic inflammation, vascular endothelial cell dysfunction, and progressive tissue fibrosis of the skin and internal organs. Moreover, increased cancer incidence and accelerated aging are also found. The increased cancer incidence is believed to be a result of chromosome instability. Accelerated cellular senescence has been confirmed by the shortening of telomere length due to increased DNA breakage, abnormal DNA repair response, and telomerase deficiency mediated by enhanced oxidative/nitr

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Liermann-Wooldrik, Kia T., Elizabeth A. Kosmacek, Joshua A. McDowell, et al. "Radiation Promotes Acute and Chronic Damage to Adipose Tissue." International Journal of Molecular Sciences 26, no. 12 (2025): 5626. https://doi.org/10.3390/ijms26125626.

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Radiotherapy is commonly used for treating various types of cancer. In addition, adipose tissue is not routinely spared during typical radiation treatment. Although radiation is known to induce metabolic effects in patients, the effects of radiation therapy on adipose tissue have not been elucidated. Currently, few studies have investigated the impact of radiation exposure on adipose tissue, and these have primarily involved whole-body irradiation. This study aimed to understand the acutely persistent damage caused by clinically relevant radiation doses in adipocytes. Specifically, in vitro an

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Maharajan, Nagarajan, and Gwang-Won Cho. "Camphorquinone Promotes the Antisenescence Effect via Activating AMPK/SIRT1 in Stem Cells and D-Galactose-Induced Aging Mice." Antioxidants 10, no. 12 (2021): 1916. http://dx.doi.org/10.3390/antiox10121916.

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Terpenoids are a wide class of secondary metabolites with geroprotective properties that can alter the mechanism of aging and aging-related diseases. Camphorquinone (CQ) is a bicyclic monoterpenoid compound that can be efficiently synthesized through the continuous bromination and oxidation reaction of camphor. The purpose of this study is to investigate the effects of CQ on oxidative-stress-induced senescence and its underlying mechanisms. To generate oxidative stress in human bone marrow mesenchymal stem cells (hBM-MSCs) and mice, we used hydrogen peroxide (200 μM twice) and D-galactose (D-G

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Di Carlo, Emma, and Carlo Sorrentino. "Oxidative Stress and Age-Related Tumors." Antioxidants 13, no. 9 (2024): 1109. http://dx.doi.org/10.3390/antiox13091109.

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Oxidative stress is the result of the imbalance between reactive oxygen and nitrogen species (RONS), which are produced by several endogenous and exogenous processes, and antioxidant defenses consisting of exogenous and endogenous molecules that protect biological systems from free radical toxicity. Oxidative stress is a major factor in the aging process, contributing to the accumulation of cellular damage over time. Oxidative damage to cellular biomolecules, leads to DNA alterations, lipid peroxidation, protein oxidation, and mitochondrial dysfunction resulting in cellular senescence, immune

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Holvoet, Paul. "Aging and Metabolic Reprogramming of Adipose-Derived Stem Cells Affect Molecular Mechanisms Related to Cardiovascular Diseases." Cells 12, no. 24 (2023): 2785. http://dx.doi.org/10.3390/cells12242785.

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We performed a systematic search of the PubMed database for English-language articles related to the function of adipose-derived stem cells in the pathogenesis of cardiovascular diseases. In preclinical models, adipose-derived stem cells protected arteries and the heart from oxidative stress and inflammation and preserved angiogenesis. However, clinical trials did not reiterate successful treatments with these cells in preclinical models. The low success in patients may be due to aging and metabolic reprogramming associated with the loss of proliferation capacity and increased senescence of st

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Denu, Ryan A., and Peiman Hematti. "Effects of Oxidative Stress on Mesenchymal Stem Cell Biology." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/2989076.

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Mesenchymal stromal/stem cells (MSCs) are multipotent stem cells present in most fetal and adult tissues.Ex vivoculture-expanded MSCs are being investigated for tissue repair and immune modulation, but their full clinical potential is far from realization. Here we review the role of oxidative stress in MSC biology, as their longevity and functions are affected by oxidative stress. In general, increased reactive oxygen species (ROS) inhibit MSC proliferation, increase senescence, enhance adipogenic but reduce osteogenic differentiation, and inhibit MSC immunomodulation. Furthermore, aging, sene

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Lettieri-Barbato, Daniele, Katia Aquilano, Carolina Punziano, Giuseppina Minopoli, and Raffaella Faraonio. "MicroRNAs, Long Non-Coding RNAs, and Circular RNAs in the Redox Control of Cell Senescence." Antioxidants 11, no. 3 (2022): 480. http://dx.doi.org/10.3390/antiox11030480.

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Cell senescence is critical in diverse aspects of organism life. It is involved in tissue development and homeostasis, as well as in tumor suppression. Consequently, it is tightly integrated with basic physiological processes during life. On the other hand, senescence is gradually being considered as a major contributor of organismal aging and age-related diseases. Increased oxidative stress is one of the main risk factors for cellular damages, and thus a driver of senescence. In fact, there is an intimate link between cell senescence and response to different types of cellular stress. Oxidati

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Mas-Bargues, Cristina, Consuelo Borrás, and Jose Viña. "Bcl-xL as a Modulator of Senescence and Aging." International Journal of Molecular Sciences 22, no. 4 (2021): 1527. http://dx.doi.org/10.3390/ijms22041527.

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Many features of aging result from the incapacity of cells to adapt to stress conditions. When cells are overwhelmed by stress, they can undergo senescence to avoid unrestricted growth of damaged cells. Recent findings have proven that cellular senescence is more than that. A specific grade of senescence promotes embryo development, tissue remodeling and wound healing. However, constant stresses and a weakening immune system can lead to senescence chronicity with aging. The accumulation of senescent cells is directly related to tissue dysfunction and age-related pathologies. Centenarians, the

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Salmon, Adam, Roy Liu, Daniel Pulliam, and Arlan Richardson. "Depot-Specific Patterns in Adipose Tissue Oxidative Stress and Dysfunction during Aging." Free Radical Biology and Medicine 65 (November 2013): S117. http://dx.doi.org/10.1016/j.freeradbiomed.2013.10.685.

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Lee, Jong-Sun, Yan Mo, Haiyun Gan, et al. "Pak2 kinase promotes cellular senescence and organismal aging." Proceedings of the National Academy of Sciences 116, no. 27 (2019): 13311–19. http://dx.doi.org/10.1073/pnas.1903847116.

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Cellular senescence defines an irreversible cell growth arrest state linked to loss of tissue function and aging in mammals. This transition from proliferation to senescence is typically characterized by increased expression of the cell-cycle inhibitor p16INK4a and formation of senescence-associated heterochromatin foci (SAHF). SAHF formation depends on HIRA-mediated nucleosome assembly of histone H3.3, which is regulated by the serine/threonine protein kinase Pak2. However, it is unknown if Pak2 contributes to cellular senescence. Here, we show that depletion of Pak2 delayed oncogene-induced

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Sekiya, Felipe Seiti, and Suely Kazue Nagahashi Marie. "Mitochondriogenesis and brain aging." Revista de Medicina 97, Suppl.1 (2018): 21–22. http://dx.doi.org/10.11606/issn.1679-9836.v97isuppl.1p21-22.

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Introduction: Mitochondriogenesis is the cellular process responsible for the generation of new mitochondria and consists of the replication of mitochondrial DNA (mtDNA) and the organelle division. Several studies suggest mitochondriogenesis is regulated by oxidative stress through a molecular pathway that involves the peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and the mitochondrial transcription factors A, B1 and B2 (TFAM, TFB1M, TFB2M). According to the Mitochondrial Theory of Aging, reactive oxygen species (ROS) generated in oxidative phosphorylation damag

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Trnovska, Jaroslava, Petr Svoboda, Helena Pelantova, et al. "Complex Positive Effects of SGLT-2 Inhibitor Empagliflozin in the Liver, Kidney and Adipose Tissue of Hereditary Hypertriglyceridemic Rats: Possible Contribution of Attenuation of Cell Senescence and Oxidative Stress." International Journal of Molecular Sciences 22, no. 19 (2021): 10606. http://dx.doi.org/10.3390/ijms221910606.

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(1) Background: empagliflozin, sodium-glucose co-transporter 2 (SGLT-2) inhibitor, is an effective antidiabetic agent with strong cardio- and nephroprotective properties. The mechanisms behind its cardio- and nephroprotection are still not fully clarified. (2) Methods: we used male hereditary hypertriglyceridemic (hHTG) rats, a non-obese model of dyslipidaemia, insulin resistance, and endothelial dysfunction fed standard diet with or without empagliflozin for six weeks to explore the molecular mechanisms of empagliflozin effects. Nuclear magnetic resonance (NMR)-based metabolomics; quantitativ

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Rivas, Melissa, Gayatri Gupta, Louis Costanzo, Huma Ahmed, Anne E. Wyman, and Patrick Geraghty. "Senescence: Pathogenic Driver in Chronic Obstructive Pulmonary Disease." Medicina 58, no. 6 (2022): 817. http://dx.doi.org/10.3390/medicina58060817.

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Chronic obstructive pulmonary disease (COPD) is recognized as a disease of accelerated lung aging. Over the past two decades, mounting evidence suggests an accumulation of senescent cells within the lungs of patients with COPD that contributes to dysregulated tissue repair and the secretion of multiple inflammatory proteins, termed the senescence-associated secretory phenotype (SASP). Cellular senescence in COPD is linked to telomere dysfunction, DNA damage, and oxidative stress. This review gives an overview of the mechanistic contributions and pathologic consequences of cellular senescence i

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Zhou, Huakang, Xuanchen Li, Majeed Rana, Jan Frederick Cornelius, Dilaware Khan, and Sajjad Muhammad. "mTOR Inhibitor Rapalink-1 Prevents Ethanol-Induced Senescence in Endothelial Cells." Cells 12, no. 22 (2023): 2609. http://dx.doi.org/10.3390/cells12222609.

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The cardiovascular risk factors, including smoking, ethanol, and oxidative stress, can induce cellular senescence. The senescent cells increase the expression and release of pro-inflammatory molecules and matrix metalloproteinase (MMPs). These pro-inflammatory molecules and MMPs promote the infiltration and accumulation of inflammatory cells in the vascular tissue, exacerbating vascular tissue inflammation. MMPs damage vascular tissue by degenerating the extracellular matrix. Consequently, these cellular and molecular events promote the initiation and progression of cardiovascular diseases. We

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