{"title":"Variety of sleep and circadian rhythms of elderly dementia patients living in group home residences.","authors":"Naoko Kubota, Noriko Matsuura, Maiko Ebina, Hitomi Suzuki, Nagomi Miyagi, Naoki Masukawa, Fumihiro Kouga, Yujiro Yamanaka","doi":"10.1007/s10522-025-10280-5","DOIUrl":"10.1007/s10522-025-10280-5","url":null,"abstract":"<p><p>In the present study, we investigated 70 elderly individuals with dementia residing in a group home in Japan (88.1 ± 6.6 SD years; 12 males and 58 females). Sleep measurements were collected via an accelerometer placed under the mattress from March 2021 to January 2024. The accelerometer-derived activity counts were transformed and plotted as actograms. On the basis of the actograms, sleep patterns were categorized into three groups: regular nighttime sleep (Type 1, n = 38, 54.3%), regular nighttime sleep with daytime naps (Type 2, n = 29, 41.4%), and irregular sleep (Type 3, n = 3, 4.3%). We compared accelerometer-derived sleep measures between the Type 1 and Type 2 groups due to the small number of participants in Type 3. Interestingly, Type 2 individuals had a significantly longer bed in time and total sleep time. However, their sleep onset latency, time of wakefulness after sleep onset and sleep efficiency did not differ from those of Type 1 individuals. Additionally, we assessed the relationships between sleep patterns and dementia characteristics, such as independence in daily living and level of care needed. No significant differences were observed in sleep measurements across these characteristics. To evaluate endogenous circadian rhythms, seven dementia patients (Type 1, n = 1; Type 2, n = 6) wore a patch-type wearable temperature sensor for approximately 24 h to estimate core body temperature (CBT). Although the zero-amplitude test revealed a significant rhythmicity in all patients, the CBT rhythms showed lower amplitude and unstable phases. In summary, our findings indicate that dementia patients display varying sleep patterns that are independent of dementia characteristics. The dysfunction of sleep homeostasis and entrainment of circadian pacemakers might be due to the light environment in the group home residence or impairment of the circadian clock itself in dementia patients.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"131"},"PeriodicalIF":4.1,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12204944/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144504800","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiogerontologyPub Date : 2025-06-27DOI: 10.1007/s10522-025-10266-3
QianKun Yang, Shan Zhu, YanFang Luo, HongBo Ai, Lei Feng, Li Zhang, Fei Luo
{"title":"Cholesterol's hidden impact: the nonlinear link between remnant cholesterol (RC) and phenotypic age acceleration (PhenoAgeAccel).","authors":"QianKun Yang, Shan Zhu, YanFang Luo, HongBo Ai, Lei Feng, Li Zhang, Fei Luo","doi":"10.1007/s10522-025-10266-3","DOIUrl":"10.1007/s10522-025-10266-3","url":null,"abstract":"<p><p>Cholesterol metabolism disorders have been shown to correlate with multiple physiopathologic aspects of cellular aging. However, whether indicators reflecting cholesterol metabolism [e.g., remnant cholesterol (RC)] can serve as biomarkers for biological aging remains unclear. To address this gap, this study aimed to explore the relationship between RC and phenotypic age acceleration (PhenoAgeAccel) using data from the National Health and Nutrition Examination Survey (NHANES) database. First, participants with complete information on RC, PhenoAgeAccel, and other essential covariates were included and analyzed. Subsequently, multivariable generalized linear regression models, subgroup analyses, interaction tests, and restricted cubic spline (RCS) analyses were utilized to explore the association. Results showed that a total of 4,471 participants were included for analysis. After adjusting for all potential covariates, a one-unit increase in RC was associated with a 0.724-year increase in PhenoAgeAccel (β = 0.724, 95% CI: 0.106-1.341). Notably, subgroup analyses and interaction tests further revealed a more pronounced RC-PhenoAgeAccel association in individuals with diabetes (β = 4.331, 95% CI: 1.607-7.055) and hypertension (β = 2.069, 95% CI: 0.887-3.251). In addition, RCS analysis identified a positive and nonlinear association between RC and PhenoAgeAccel (P for nonlinearity < 0.001), and threshold effect analysis determined an inflection point of 0.564 mmol/L for RC. Specifically, a positive and segmented RC-PhenoAgeAccel association was observed within the 0.564-mmol/L threshold (β = 9.653, 95% CI: 7.452-11.853), and such association remained significant beyond this point (β = 1.121, 95% CI: 0.193-2.049). In conclusion, RC was positively and nonlinearly associated with accelerated aging. Thus, controlling RC below 0.564 mmol/L might contribute to anti-aging effects and thereby help prevent aging-related diseases.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"133"},"PeriodicalIF":4.1,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144511507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiogerontologyPub Date : 2025-06-27DOI: 10.1007/s10522-025-10281-4
Avnish Kumar Verma, Sandeep Singh, Syed Ibrahim Rizvi
{"title":"Circadian clock and its effect on aging and lifespan.","authors":"Avnish Kumar Verma, Sandeep Singh, Syed Ibrahim Rizvi","doi":"10.1007/s10522-025-10281-4","DOIUrl":"10.1007/s10522-025-10281-4","url":null,"abstract":"<p><p>The circadian clocks of the cell orchestrate a daily transcriptional rhythm that schedules key activities of the cell to maintain homeostasis and support resilience. Circadian rhythm is driven by the periodic oscillations of transcriptional activators and translational repressors, occurring in both the central and peripheral clocks. Accumulating evidence shows that aging impairs the functional synchrony of the circadian system which further escalate age-related disorders. In addition, the technological aspects of modern society, including constant work schedules and extensive use of personal electronics, have led to a significant rise in circadian disorders. Circadian dysfunction seems to adversely impact aging and longevity in animal models. Therefore, it is essential to conduct comprehensive studies to identify factors that worsen with aging and to discover therapeutic options for promoting healthy aging. This review examines how aging affects circadian function and the reciprocal effects of circadian disruption (CD) on aging and longevity. Further, we highlight the recent findings on non-pharmacological aspects such as dietary restrictions and physical exercise as a regulator of circadian rhythms, aging attenuation, and extending lifespan in mammals. Thus, resetting the circadian clock may lead to better synchrony in cellular homeodynamics and physiology which offers healthy aging and increased life span.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"132"},"PeriodicalIF":4.1,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144504798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiogerontologyPub Date : 2025-06-25DOI: 10.1007/s10522-025-10274-3
Omidreza Salehi, Dariush Sheikholeslami-Vatani, Seyed Ali Hosseini
{"title":"Positive effects of HIIT and vitamin E on cognitive function, angiogenesis and NRF2 antioxidant pathway in male rats with Alzheimer's disease.","authors":"Omidreza Salehi, Dariush Sheikholeslami-Vatani, Seyed Ali Hosseini","doi":"10.1007/s10522-025-10274-3","DOIUrl":"10.1007/s10522-025-10274-3","url":null,"abstract":"<p><p>Interactive effects of exercise and antioxidant supplements are still not well known. So, The aim of this study was to investigate the effects of high intensity interval training (HIIT) and vitamin E (VE) on the PI3K/NRF2 pathway in the hippocampus of Alzheimer's disease rats (AD). In this expremantal study, fifty aged AD rats with 10 mg/kg trimethyltin (TMT), were divided into groups 1) TMT, 2) VE solvent (Sham), 3) VE (30 mg/kg), 4) HIIT (90-95% of the maximum running speed) and 5) HIIT+VE. Ten healthy rats were included in the healthy control group to investigate the effect of TMT on research variables. Results Showed that, HIIT, VE and HIIT+VE decreased amyloid beta (P≤0.05), HIIT and HIIT+VE decreased NF-kB (P≤0.05) as well as HIIT, VE and HIIT+VE increased SOD and decreased MDA. HIIT simultaneously with VE increased PI3K, NRF2, and Cat. HIIT, VE and the interaction of HIIT and VE decreased the expression of miR-125b and increased expression of miR-132 (P≤0.05); The combination of HIIT and VE increased capillary density in areas 1 and 3, the percentage of healthy cells in C1 and C3 areas of the hippocampus (P≤0.05). The effects of HIIT and HIIT+VE on improving memory were better than VE (P≤0.05). It seems that HIIT and VE can synergistically increase the expression of antioxidant genes from the PI3K/NRF2 pathway by decreasing miR-125 and increasing miR-132. Probably, this happens by reducing some AD markers, increasing angiogenesis and cell protection as well as cognitive memory in AD situation.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"129"},"PeriodicalIF":4.1,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144494086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Mechanisms of endothelial senescence and vascular aging.","authors":"Qiao Li, Zonghao Qian, Yuzhen Huang, Xiao Yang, Jiankun Yang, Nanyin Xiao, Guangyu Liang, Heng Zhang, Yanguang Fu, Yan Lin, Cuntai Zhang, Anding Liu","doi":"10.1007/s10522-025-10279-y","DOIUrl":"10.1007/s10522-025-10279-y","url":null,"abstract":"<p><strong>Scope: </strong>Cardiovascular disease (CVD) is a major cause of mortality, especially in the aging population. Aging is one of the main risk factors contributing to CVD, leading to early mortality and a decline in the quality of life. Vascular aging is closely linked with atherosclerosis, diabetes, hypertension, stroke, heart failure, and peripheral arterial diseases. Elucidating the cellular and molecular mechanisms underlying vascular aging help to develop therapeutic strategies that can address age-related vascular diseases and decrease the rate of morbidity and mortality among the older population. Endothelial cells located on the interior layer of blood vessels. Intima layers of vascular vessels are damaged and remodeled during vascular aging. The dysfunction of smooth muscle cells and endothelial cells plays key roles in vascular aging. Common pathological changes during vascular aging include arterial stiffness, calcification, and atherosclerosis. Endothelial cell senescence is driven by complex underlying mechanisms. The complex regulation of aging and antiaging network in endothelial cells involve several factors, such as Klotho protein, nitric oxide, fibroblast growth factor 21 (FGF21), and SIRT family members.</p><p><strong>Objectives: </strong>This review aims to systematically delineate the mechanisms underlying the endothelial senescence.</p><p><strong>Methodology: </strong>The publications on the endothelial cell senescence mechanisms and its roles in vascular aging and aging related diseases are comprehensively investigated and summarized. In this review, the roles of various components in endothelial cell senescence are discussed to elucidate the underlying molecular mechanisms of endothelial cell senescence and identify potential therapeutic targets.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"128"},"PeriodicalIF":4.1,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144483027","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Elucidating the anti-aging bioactive compounds and mechanisms of Jingfang Granules formula based on network pharmacology and Caenorhabditis elegans.","authors":"Rui Zhao, Taili Zhao, Tingting Shi, Chuanjiao Feng, Honghua Li, Ying Xu, Qingqing Zhang, Xin Yin, Jingchun Yao, Guimin Zhang, Xuekui Xia","doi":"10.1007/s10522-025-10276-1","DOIUrl":"10.1007/s10522-025-10276-1","url":null,"abstract":"<p><p>Jingfang Granule (JFG), a traditional Chinese medicine preparation, is widely used in clinical practice. It has been shown to extend both lifespan and healthspan in the Caenorhabditis elegans model. However, the molecular mechanisms of its main constituents and their targets remain unclear. In this study, through network pharmacology, molecular docking, and experiments on C. elegans including lifespan assays and stress resistance assays, the bioactive compounds of JFG and their targets were screened. Network analysis identified a total of 187 candidate components and 150 drug-disease related targets, among which TP53, STAT3, IL6, TNF, AKT1, ESR1, CCND1, BCL2, MAPK1, and MAPK3 were the core nodes. Gene Ontology (GO) enrichment analysis revealed that these targets were mainly involved in aging-related and anti-apoptotic processes. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis suggested that the AGE-RAGE signaling pathway, which is crucial in diabetic complications, might be involved. Experiments on Caenorhabditis elegans further confirmed that neohesperidin, kaempferol, and stigmasterol in Jingfang Granule exhibited good anti-aging effects and stress resistance. They could extend the lifespan of Caenorhabditis elegans by activating the target genes of the transcription factors DAF-16, HSF-1, and SKN-1. By combining the strategies of network pharmacology and molecular biology, this study elucidated the anti-aging mechanisms of the Jingfang Granule formula and its bioactive compounds. Therefore, the Jingfang Granule formula and its bioactive compounds hold potential for lifespan extension, healthspan improvement, and enhanced stress resistance.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"127"},"PeriodicalIF":4.1,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144473882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiogerontologyPub Date : 2025-06-24DOI: 10.1007/s10522-025-10269-0
Sakshi Chaudhary, Mani Raj Chaudhary, Manoj Kumar Jena, Prasana Kumar Rath, Bidyut Prava Mishra, Biswaranjan Paital, Ashish Vyas, Dipak Kumar Sahoo, Prabhakar Singh, Mohammad Murtaza Mehdi
{"title":"Calorie restriction mimetics against aging and inflammation.","authors":"Sakshi Chaudhary, Mani Raj Chaudhary, Manoj Kumar Jena, Prasana Kumar Rath, Bidyut Prava Mishra, Biswaranjan Paital, Ashish Vyas, Dipak Kumar Sahoo, Prabhakar Singh, Mohammad Murtaza Mehdi","doi":"10.1007/s10522-025-10269-0","DOIUrl":"10.1007/s10522-025-10269-0","url":null,"abstract":"<p><p>Geroprotectors, a class of compounds that ameliorate molecular, cellular, or physiological aging-related alterations, have garnered significant attention in the quest to promote healthy aging and extend the human health span. Among these, Calorie Restriction Mimetics (CRMs) have emerged as promising candidates due to their potential to mimic the benefits of calorie restriction, a dietary approach involving reduced calorie intake without malnutrition. Prospective CRMs may include biguanides (metformin and aminoguanidine), which exert effects on the insulin signaling pathway; rapamycin, which interacts with mTOR signaling pathways; and stilbenes (resveratrol), which influences stress signaling pathways and promotes the activation of AMPK, impacting mitochondrial metabolism in addition to the activity of FOXO and sirtuin. Other compounds, such as glycolytic inhibitors, carbohydrate and lipid absorption blockers, polyamines, and polyphenols, which collectively modulate pathways regulating the effects of free radicals, are also under consideration. To propose prospective geroprotective strategies, this article focuses on analyzing the functions of potential CRMs and their mechanisms demonstrating health benefits, the same as that of CR (Calorie Restriction), but without undesirable side effects.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"126"},"PeriodicalIF":4.1,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144473881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Unveiling mysteries of aging: the potential of melatonin in preventing neurodegenerative diseases in older adults.","authors":"Omer Unal, Nilufer Akgun-Unal, Abdulkerim Kasim Baltaci","doi":"10.1007/s10522-025-10254-7","DOIUrl":"10.1007/s10522-025-10254-7","url":null,"abstract":"<p><p>Neurodegenerative conditions, including Alzheimer's disease, Parkinson's disease, and Huntington's disease, result in a substantial health problem for the elderly, marked by ongoing neuronal degeneration and a deterioration in mental faculties. These disorders are frequently linked to oxidative stress, problems with mitochondria, and persistent inflammation in the brain, which worsen neuronal damage. The neurohormone melatonin, primarily secreted by the pineal gland, has gained recognition as a promising therapeutic agent due to its antioxidant, anti-inflammatory, and neuroprotective effects. Melatonin's functions extend beyond its regulation of circadian rhythms, as research has demonstrated its ability to remove free radicals, improve mitochondrial performance, and adjust immune system responses, ultimately reducing the progression of neurodegenerative disease. Research findings from preclinical and clinical trials imply that taking melatonin supplements could lead to improved cognitive abilities, slower disease progression, and an overall better quality of life for elderly individuals suffering from neurodegenerative conditions. The mechanisms through which melatonin acts, the best dosage, and its long-term effectiveness are still being researched. This review underscores the potential benefits of melatonin as a supplementary treatment for neurodegenerative disorders in older adults, stressing the necessity for additional studies to confirm its efficacy and standardize its use in treatment plans.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"125"},"PeriodicalIF":4.1,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12187872/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144473916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Biological properties, synthetic pathways and anti-aging mechanisms of nicotinamide mononucleotide (NMN): Research progress and challenges.","authors":"Enhui Wang, Yuting Wang, Zhaofeng Zhang, Yanfei Jiang, Chunyue Zhao","doi":"10.1007/s10522-025-10270-7","DOIUrl":"10.1007/s10522-025-10270-7","url":null,"abstract":"<p><p>The increasing global population aging has made the prevention and control of aging-related diseases a major public health challenge in the twenty-first century. Nicotinamide mononucleotide (NMN), as a precursor of nicotinamide adenine dinucleotide (NAD<sup>+</sup>), has garnered significant attention in recent years for its anti-aging potential. This review comprehensively reviews the metabolic pathways and molecular mechanisms of NMN, comparing the technical characteristics and industrialization prospects of chemical synthesis, microbial fermentation, and enzyme-catalyzed synthesis. The molecular targets and networks of NMN in core aging mechanisms, such as DNA damage repair, mitochondrial function regulation, inflammatory response balance, gut microbiota remodeling, and autophagy pathway activation, are analyzed. The molecular mechanism of NMN in slowing down the aging process through multi-target synergistic effects is elucidated. However, critical issues such as age-stratified dosage modeling, long-term safety, and efficacy of NMN still require in-depth research. This review provides a theoretical basis and research direction for translational research and precise anti-aging strategies of NMN.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"124"},"PeriodicalIF":4.1,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144473880","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiogerontologyPub Date : 2025-06-20DOI: 10.1007/s10522-025-10268-1
Antero Salminen, Kai Kaarniranta, Anu Kauppinen
{"title":"Photoaging: UV radiation-induced cGAS-STING signaling promotes the aging process in skin by remodeling the immune network.","authors":"Antero Salminen, Kai Kaarniranta, Anu Kauppinen","doi":"10.1007/s10522-025-10268-1","DOIUrl":"10.1007/s10522-025-10268-1","url":null,"abstract":"<p><p>Excessive exposure of the skin to UV radiaton (UVR) accelerates the aging process and leads to a photoaging state which involves similar pathological alterations to those occurring in chronological aging. UVR exposure, containing both UVA and UVB radiation, triggers cellular senescence and a chronic inflammatory state in skin. UVR promotes oxidative stress and a leakage of double-stranded DNA (dsDNA) from nuclei and mitochondria into the cytoplasm of keratinocytes and fibroblasts. It is recognized that cytosolic dsDNA is a specific danger signal which stimulates cytoplasmic DNA sensors. The activation of the signaling through the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) is a major defence and survival mechanism combatting against tissue injuries. There is abundant evidence that UVR exposure of skin stimulates cGAS-STING signaling which promotes cellular senescence and remodels both the local and systemic immune network. cGAS-STING signaling activates the IRF3 and NF-κB signaling pathways which trigger both pro-inflammatory and immunosuppressive responses. Moreover, cGAS-STING signaling stimulates inflammatory responses by activating the NLRP3 inflammasomes. Senescent fibroblasts secrete not only cytokines but also chemokines and colony-stimulating factors which induce myeloid differentiation and recruitment of immune cells into inflamed skin. Photoaging is associated with an immunosuppressive state in skin which is attributed to an expansion of immunosuppressive cells, such as Tregs. UVR-induced cGAS-STING signaling also stimulates the expression of PD-L1, a ligand for inhibitory immune checkpoint receptor, which evokes an exhaustion of effector immune cells. There is clear evidence that cGAS-STING signaling can also accelerate chronological aging by remodeling the immune network.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"123"},"PeriodicalIF":4.1,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12181222/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144336301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}