The Pivotal Role of One-Carbon Metabolism in Neoplastic Progression During the Aging Process DOI Creative Commons
Avisek Majumder,

Shabana Bano,

Kasturi Bala Nayak

et al.

Biomolecules, Journal Year: 2024, Volume and Issue: 14(11), P. 1387 - 1387

Published: Oct. 31, 2024

One-carbon (1C) metabolism is a complex network of metabolic reactions closely related to producing 1C units (as methyl groups) and utilizing them for different anabolic processes, including nucleotide synthesis, methylation, protein reductive metabolism. These pathways support the high proliferative rate cancer cells. While drugs that target (like methotrexate) have been used treatment, they often significant side effects. Therefore, developing new with minimal effects necessary effective treatment. Methionine, glycine, serine are main three precursors vital not only cells but also non-proliferative in regulating energy homeostasis aging process. Understanding potential role crucial advancing our knowledge neoplastic progression. This review provides comprehensive understanding molecular complexities context aging, paving way researchers explore avenues advanced therapeutic interventions cancer.

Language: Английский

α-arbutin prevents UVA-induced skin photodamage via alleviating DNA damage and collagen degradation in NIH-3 T3 cells DOI Creative Commons
Nan Zhao,

Xin Nie,

Yizhen Yan

et al.

Journal of Photochemistry and Photobiology B Biology, Journal Year: 2025, Volume and Issue: 263, P. 113100 - 113100

Published: Jan. 7, 2025

Ultraviolet radiation (UV) causes certain side effects to the skin, and their accumulation a extent can lead accelerated aging of skin. Recent studies suggest that α-arbutin may be useful in various disorders such as hyperpigmentation disorders, wound healing, antioxidant activity. However, role skin photodamage is unclear. In this study, under UVA-induced conditions, treated mouse fibroblasts (NIH-3T3) repair DNA damage resist apoptosis by reducing production reactive oxygen species (ROS) increasing phosphorylation glycogen synthase kinase 3 beta (GSK3β) orchestra AKT/GSK3β pathway. Meanwhile, also regulate collagen metabolism facilitate replenishment targeting SMAD3 mediate TGFβ/SMAD pathway NIH-3T3. conclusion, we found mitigate detrimental induced UVA irradiation, provides theoretical basis for use treatment photodamage.

Language: Английский

Citations

1
Harnessing Gasotransmitters to Combat Age-Related Oxidative Stress in Smooth Muscle and Endothelial Cells DOI Creative Commons
Constantin Munteanu, Anca‐Irina Galaction, Gelu Onose

et al.

Pharmaceuticals, Journal Year: 2025, Volume and Issue: 18(3), P. 344 - 344

Published: Feb. 27, 2025

Age-related oxidative stress is a critical factor in vascular dysfunction, contributing to hypertension and atherosclerosis. Smooth muscle cells endothelial are particularly susceptible damage, which exacerbates aging through cellular senescence, chronic inflammation, arterial stiffness. Gasotransmitters—hydrogen sulfide (H2S), nitric oxide (NO), carbon monoxide (CO)—are emerging as promising therapeutic agents for counteracting these processes. This review synthesizes findings from recent studies focusing on the mechanisms by H2S, NO, CO influence smooth cell function. Therapeutic strategies involving exogenous gasotransmitter delivery systems combination therapies were analyzed. H2S enhances mitochondrial bioenergetics, scavenges ROS, activates antioxidant pathways. NO improves function, promotes vasodilation, inhibits platelet aggregation. exhibits cytoprotective anti-inflammatory effects modulating heme oxygenase activity ROS production. In preclinical studies, gasotransmitter-releasing molecules (e.g., NaHS, SNAP, CORMs) targeted show significant promise. Synergistic with lifestyle modifications further enhance their potential. conclusion, gasotransmitters hold promise combat age-related cells. Their multifaceted innovative approaches make them potential candidates treating dysfunction promoting healthy aging. Further research needed translate into clinical applications.

Language: Английский

Citations

1
Exploration of the mechanism and therapy of ovarian aging by targeting cellular senescence DOI Creative Commons
Weicheng Tang, Kaichen Wang, Yourong Feng

et al.

Life Medicine, Journal Year: 2025, Volume and Issue: 4(1)

Published: Jan. 23, 2025

The ovary is a crucial gonadal organ that supports female reproductive and endocrine functions. Ovarian aging can result in decreased fertility dysfunction across multiple organs. Research has demonstrated cellular senescence various cell types within the trigger decline ovarian function through distinct stress responses, resulting aging. This review explores how may contribute to failure. Additionally, we discuss factors cause senescence, including accumulation of advanced glycation end products, oxidative stress, mitochondrial dysfunction, DNA damage, telomere shortening, exposure chemotherapy. Furthermore, six types, oocytes, granulosa cells, theca immune surface epithelium, endothelial inside explore their contribution accelerated Lastly, describe potential senotherapeutics for treatment offer novel strategies longevity.

Language: Английский

Citations

0
Involvement of TGF-β, mTOR, and inflammatory mediators in aging alterations during myxomatous mitral valve disease in a canine model DOI
Arkadiusz Grzeczka, Szymon Graczyk, Paweł Kordowitzki

et al.

GeroScience, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 26, 2025

Language: Английский

Citations

0
Targeting p53-p21 signaling to enhance mesenchymal stem cell regenerative potential DOI
Ahsas Goyal, Muhammad Afzal, Nawaid Hussain Khan

et al.

Regenerative Therapy, Journal Year: 2025, Volume and Issue: 29, P. 352 - 363

Published: April 8, 2025

Language: Английский

Citations

0
The oxidative-stress-senescence axis in keratoconus: new insights into corneal degeneration DOI Creative Commons
Maria Laura Passaro, Michele Rinaldi,

Valentina Morgera

et al.

Frontiers in Molecular Biosciences, Journal Year: 2025, Volume and Issue: 12

Published: April 24, 2025

Keratoconus is a bilateral and asymmetric degenerative eye disease that causes corneal thinning bowing, leading to irregular astigmatism vision loss. Although environmental genetic factors contribute the disease's development, exact cause underlying pathological mechanism remain unknown. In this review, we comprehensively explore latest pathophysiological mechanisms of keratoconus, focusing on oxidative damage inflammation. Senescence emerges as key driver keratoconus pathogenesis. Understanding these common elements enhances our understanding paves way for innovative therapeutic approaches keratoconus.

Language: Английский

Citations

0
Multi-pathway blood biomarkers to target and monitor multidimensional prevention of cognitive and functional decline (nested in the IN-TeMPO study framed within the world-wide FINGERS network) DOI Creative Commons
Gessica Sala, Luca Cuffaro, Federico Emanuele Pozzi

et al.

Frontiers in Aging Neuroscience, Journal Year: 2025, Volume and Issue: 17

Published: May 7, 2025

As the population ages, identification of preventive strategies able to delay cognitive and functional decline associated with aging represents a major challenge. To date, multidimensional approaches seem be effective in reducing or delaying onset age-related diseases. The multicentric randomized controlled trial IN-TeMPO (ItaliaN study Tailored Multidomain interventions Prevent community-dwelling Older adults, ClinicalTrials.gov ID NCT06248723), framed within World-Wide FINGERS network, aims verify efficacy guided multidomain preventing decline. Within this study, we will explore comprehensive array established exploratory blood biomarkers several pathologic processes, including Alzheimer's disease (AD), neurodegeneration, inflammation, senescence sarcopenia, stratify subject risk assess effect on biomarkers. ApoE4 status plasma p-tau217 NfL (neurodegeneration), GFAP IL-6 (inflammation), GDF-15 (senescence/sarcopenia) evaluated all subjects (n = 1,662) both at baseline end (12 months). Exploratory additional measured same time points subgroup 100 subjects: BDNF, ghrelin, IGF-1, irisin redox as markers sarcopenia/senescence oxidative stress, gamma-H2AX PBMCs marker senescence, amyloid beta aggregates plasma, urine erythrocytes supportive AD. Untargeted metabolomics analysis untargeted volatilomics whole performed molecular alterations that may pathogenesis progression diseases frail older adults aim identifying novel potential clinical use multiple laboratory can contribute early trajectories mechanisms underlying multidisciplinary pathological processes.

Language: Английский

Citations

0
From rest to repair: Safeguarding genomic integrity in quiescent cells DOI Creative Commons

Chin Wei Brian Leung,

Jacob Wall,

Fumiko Esashi

et al.

DNA repair, Journal Year: 2024, Volume and Issue: 142, P. 103752 - 103752

Published: Aug. 20, 2024

Quiescence is an important non-pathological state in which cells pause cell cycle progression temporarily, sometimes for decades, until they receive appropriate proliferative stimuli. Quiescent make up a significant proportion of the body, and maintaining genomic integrity during quiescence crucial tissue structure function. While are spared from DNA damage associated with replication or mitosis, still exposed to various sources endogenous damage, including those induced by normal transcription metabolism. As such, it vital that retain their capacity effectively repair lesions may occur return without losing cellular properties. Notably, while pathways often found be downregulated quiescent cells, emerging evidence suggests presence active differentially regulated mechanisms. This review aims provide current understanding processes mammalian systems sheds light on potential pathological consequences inefficient inaccurate cells.

Language: Английский

Citations

2
Senescence-Induced Atherosclerosis: The Potency of Senolytic Therapy DOI Open Access

Udani Sari Ratih,

Febriana Catur Iswanti

Bioscientia Medicina Journal of Biomedicine and Translational Research, Journal Year: 2024, Volume and Issue: 8(8), P. 4682 - 4696

Published: May 20, 2024

The aging process is an inevitable occurrence that involves physiological changes at the cellular level. presence of intrinsic and extrinsic stressors can cause damage, leading to senescence premature aging. Senescent cells undergo activation p53/p21 p16INK4a pathways, induce cell cycle arrest, increased expression senescence-associated beta-galactosidase (SA-β-Gal), secretion SASP (senescence-associated secretory phenotype), "inflamm-aging" or chronic inflammation associated with senescence. These “inflamm-aging” accelerates age-related diseases, one which atherosclerosis. relationship between aging, senescence, atherosclerosis has been a focus research on pathogenesis, prevention, therapy. Recent emphasized crucial role senolytics, compounds agents capable eliminating senescent cells, in inhibiting progression slowing down Obtaining more comprehensive understanding processes effectiveness senolytics should facilitate development potent medicines mitigate side effects management cardiovascular disease extend longevity.

Language: Английский

Citations

1
Novel Techniques for Mapping DNA Damage and Repair in the Brain DOI Open Access

Jenna Hedlich-Dwyer,

Joanne Allard,

Veronica E. Mulgrave

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(13), P. 7021 - 7021

Published: June 27, 2024

DNA damage in the brain is influenced by endogenous processes and metabolism along with exogenous exposures. Accumulation of can contribute to various neurological disorders, including neurodegenerative diseases neuropsychiatric disorders. Traditional methods for assessing brain, such as immunohistochemistry mass spectrometry, have provided valuable insights but are limited their inability map specific adducts regional distributions within or genome. Recent advancements detection offer new opportunities address these limitations further our understanding repair brain. Here, we review emerging techniques offering more precise sensitive ways detect quantify lesions neural cells. We highlight applications discuss potential determining role disease.

Language: Английский

Citations

1