Frontiers in aging最新文献

{"title":"Handgrip strength across clinical conditions and health-related outcomes in older adults: a scoping review.","authors":"José Julián Bernal-Sánchez, Duber Esteban Uzuriaga-Fori, Sharon Estefany Rivera-Viveros, Zharick Marcela Viafara-Carabali, Esther Cecilia Wilches-Luna, Diana Yazmín Perafan-Gonzalez","doi":"10.3389/fragi.2026.1804033","DOIUrl":"10.3389/fragi.2026.1804033","url":null,"abstract":"<p><strong>Background and aim: </strong>Handgrip strength (HGS) is a simple, non-invasive, and widely used measure of muscle function that has been examined in relation to several health-related outcomes in older adults. This scoping review aimed to map the extent, range, and nature of the evidence on the relationship between HGS and clinical conditions or health-related outcomes in older adults and aging-related populations, with particular attention to population characteristics, outcome classification, and HGS measurement protocols.</p><p><strong>Methods: </strong>This scoping review was reported in accordance with the PRISMA-ScR checklist. Observational studies, including cross-sectional, cohort, longitudinal, and panel designs, were eligible when they examined HGS in relation to clinical conditions or health-related outcomes in older adults or aging-related populations. Searches were conducted in ScienceDirect, Scopus, Web of Science, LILACS, SciELO, and MEDLINE via PubMed, with SpringerLink used as a supplementary publisher platform. Articles published in English, Spanish, or Portuguese were considered. Study selection, data charting, and methodological appraisal were performed using structured forms. Findings were synthesized descriptively by study characteristics, health-related domain, HGS measurement protocol, and HGS operationalization.</p><p><strong>Results: </strong>The search identified 890 records, and 18 studies comprising 243,334 participants were included in the final synthesis. Ten studies were cross-sectional, whereas eight used longitudinal, cohort, or panel designs. Neurocognitive and mental health outcomes were the most frequently examined domain, followed by musculoskeletal conditions or syndromes, functional outcomes, quality of life, frailty, comorbidity burden, and cardiovascular risk. HGS measurement varied across studies in terms of dynamometer type, hand assessed, number of attempts, summary value, cut-off points, and analytical operationalization. Lower HGS or HGS-related parameters were reported across studies in relation to poorer health-related outcomes, although study design, population heterogeneity, and differences in HGS protocols limited direct comparability.</p><p><strong>Conclusion: </strong>This review shows that HGS has been studied across multiple aging-related health domains, particularly neurocognitive and musculoskeletal outcomes. However, the predominance of observational designs and heterogeneity in HGS measurement and outcome definitions limit causal interpretation. Further longitudinal studies using standardized HGS protocols and consistent outcome definitions are needed.</p>","PeriodicalId":73061,"journal":{"name":"Frontiers in aging","volume":"7 ","pages":"1804033"},"PeriodicalIF":4.9,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13364915/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148450834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Heterogeneous leukocyte telomere trajectories and inflammatory resolution 12 months after mild COVID-19: an exploratory cohort study.","authors":"Daiane Renata Dos Santos, Daniela Valadão Freitas Rosa, Arnaldo Santos Leite, Carolina Coimbra Marinho, Maria Aparecida Camargos Bicalho, Marco Aurelio Romano-Silva, Débora Marques de Miranda, Alexandre Guimarães de Almeida Barros","doi":"10.3389/fragi.2026.1866981","DOIUrl":"10.3389/fragi.2026.1866981","url":null,"abstract":"<p><strong>Background: </strong>The longitudinal interplay between leukocyte telomere length (LTL) and persistent immune activation after mild SARS-CoV-2 infection remains incompletely characterized.</p><p><strong>Methods: </strong>In this exploratory observational study, 51 adults (76.5% female; mean age 39.0 ± 9.7 years) with RT-PCR-confirmed mild COVID-19 had blood sampled in the acute symptomatic phase and at 12 months. Relative LTL was quantified by qPCR (Cawthon T/S method, 36B4 reference). A 45-analyte multiplex bead-based immunoassay quantified circulating cytokines, chemokines and growth factors. Paired changes were assessed with Wilcoxon signed-rank tests; cross-sectional and longitudinal associations between immune mediators and LTL were evaluated by Spearman correlation with Benjamini-Hochberg false discovery rate (FDR) control and by multivariable linear regression adjusted for baseline LTL, age, sex and comorbidity burden.</p><p><strong>Results: </strong>Forty-eight participants had paired LTL data. Group-level T/S ratio increased modestly between the acute phase and 12 months (mean Δ = +0.0094; Wilcoxon p = 0.041; Cohen's d_z = 0.31), but interindividual trajectories were markedly heterogeneous (52% increased, 33% decreased, 15% unchanged). Twenty of 45 cytokines decreased significantly between timepoints (FDR <0.05), consistent with systemic resolution of acute inflammation. Among residual immune mediators at 12 months, hepatocyte growth factor (HGF) was inversely associated with the LTL trajectory (Spearman ρ = -0.48; p = 0.0005; FDR = 0.024). This association persisted in a multivariable model adjusted for baseline LTL, age, sex and comorbidity count (β = -0.040; 95% CI -0.061 to -0.018; p = 0.0006), and the model explained 43% of variance in T/S₁. Cytokines previously highlighted in similar cohorts (IL-7, IL-9, IL-17A, EGF) showed univariable correlations that did not survive FDR correction.</p><p><strong>Conclusion: </strong>Twelve months after mild SARS-CoV-2 infection, leukocyte telomere trajectories are highly individual, while most acute-phase inflammatory mediators have resolved. Residual circulating HGF, a pleiotropic factor recognized as a component of the senescence-associated secretory phenotype but also involved in tissue repair, endothelial activation, and metabolic signaling, was the only mediator robustly associated with the longitudinal LTL trajectory after multiple-testing correction and may identify a subgroup with persistent tissue-remodeling or senescence-associated activity. This association is interpreted as exploratory and hypothesis-generating rather than as a validated biomarker. Given the absence of an uninfected control group, modest sample size, and qPCR-based LTL quantification, these findings should be interpreted as hypothesis-generating.</p>","PeriodicalId":73061,"journal":{"name":"Frontiers in aging","volume":"7 ","pages":"1866981"},"PeriodicalIF":4.9,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13367134/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148450891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanistic redundancy and hierarchy of aging mechanisms: implications for strategies to extend healthspan and biomarker integration.","authors":"Maria Shvedova","doi":"10.3389/fragi.2026.1776669","DOIUrl":"10.3389/fragi.2026.1776669","url":null,"abstract":"<p><p>Aging involves a network of interrelated biological processes that differ in causality and impact. This review proposes a hierarchical framework of primary, secondary, and tertiary drivers of human aging while emphasizing the extensive feedback loops and mechanistic redundancy. Primary mechanisms include molecular damage, particularly genomic and mitochondrial DNA damage, and mutation accumulation that cumulatively result in genomic instability, and telomere attrition, which represents a separate primary driver. Although rarely recognized as an independent aging mechanism, female sex hormone decline, particularly the abrupt loss of sex steroid signaling at menopause and earlier perimenopausal changes, may constitute a primary sex-specific driver of human aging as an evolved process that amplifies molecular and physiological deterioration. Mechanisms acting as both primary and secondary include damage to molecules other than DNA including protein damage with loss of proteostasis and lipid damage, which may arise directly from molecular insults or emerge as downstream consequences of DNA damage and other primary mechanisms, while also feeding back to accelerate upstream deterioration. Secondary mechanisms comprise cellular senescence, impaired macroautophagy, deregulated nutrient sensing, epigenetic alterations, mitochondrial dysfunction, and altered intercellular communication. These processes emerge downstream of initial damage and further reciprocally reinforce it. Tertiary mechanisms of aging comprise stem cell exhaustion, chronic inflammation, and dysbiosis, which represent the system-level deterioration exacerbating molecular dysfunction. This hierarchical network-based model suggests that many hallmarks of aging may represent manifestations of redundant upstream molecular insults. This review focuses on primary mechanisms as the causative drivers of aging and proposes that the strategy to extend healthspan may require preventive approaches targeting distinct redundant primary mechanisms. Complex preventive interventions that simultaneously reduce molecular damage, slow telomere attrition, and compensate for estrogen depletion may delay the initiation and amplification of secondary and tertiary aging mechanisms. This framework supports coordinated multi-target strategies for healthspan extension and underscores the need for validated biomarkers that reflect these upstream processes as part of an integrated preventive approach.</p>","PeriodicalId":73061,"journal":{"name":"Frontiers in aging","volume":"7 ","pages":"1776669"},"PeriodicalIF":4.9,"publicationDate":"2026-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13357817/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148439250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From molecular damage to regulatory constraint: epigenetic and metabolic limits of cellular plasticity in aging.","authors":"Antoni R Godlewski, Tomasz Dziaman","doi":"10.3389/fragi.2026.1872180","DOIUrl":"10.3389/fragi.2026.1872180","url":null,"abstract":"<p><p>Aging is most often portrayed as the progressive buildup of molecular damage, yet this conventional view leaves much unexplained. Over time, cells and tissues appear to lose the regulatory flexibility that allows them to adapt, repair, and reconfigure their functional states. Genomic instability, metabolic imbalance, mitochondrial dysfunction, and proteostatic decline converge on aging, but their effects focus on chromatin organization, transcriptional coordination, and signaling networks that maintain cellular identity. In this review, we propose that aging can be usefully viewed as a progressive restriction of epigenetic and regulatory plasticity, rather than as the simple accumulation of lesions. Pathways such as Wnt signaling, TET-dependent DNA demethylation, and metabolic sensors including AMPK, mTOR, and sirtuins create an interconnected landscape that links environmental and metabolic conditions with long-term cellular behavior. As this landscape becomes increasingly rigid and constrained, cells retain viability but lose their capacity for dynamic responses, stabilizing in low-plasticity states that include cellular senescence. Framing aging as a shift from adaptive plasticity toward regulatory rigidity offers a possible integrative lens on classical hallmarks and epigenetic aging signatures, without replacing existing models. Rather than targeting individual hallmarks in isolation, future approaches may need to complement hallmark-focused strategies by restoring dynamic balance within epigenetic and signaling networks that preserve tissue-level homeostasis and regenerative potential, thereby suggesting specific, testable predictions for interventions acting on metabolic-epigenetic axes.</p>","PeriodicalId":73061,"journal":{"name":"Frontiers in aging","volume":"7 ","pages":"1872180"},"PeriodicalIF":4.9,"publicationDate":"2026-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13350435/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148426954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Employed cancer survivors develop a peer-support intervention to improve social connections: a participatory design study.","authors":"Alicia G Dugan, Keith M Bellizzi, Hannah L Austin, Sara Namazi, Jennifer M Cavallari","doi":"10.3389/fragi.2026.1802482","DOIUrl":"10.3389/fragi.2026.1802482","url":null,"abstract":"<p><strong>Introduction: </strong>Among the 4.3 million working-age breast cancer survivors in the U.S., employment offers financial stability, purpose, and normalcy. However, many face barriers that hinder workforce participation, including social disconnection. Using a participatory intervention design approach that directly engages survivors, this study aimed to identify root causes of disconnection and prioritize solutions to support psychosocial wellbeing and work retention.</p><p><strong>Methods: </strong>This study recruited six employed breast cancer survivors for a design team that used the Intervention Design and Analysis Scorecard's (IDEAS) Steps 1-5 to develop and prioritize intervention options. The team, facilitated by university researchers, met for seven 1-h sessions. Qualitative data from IDEAS worksheets and meeting notes were analyzed.</p><p><strong>Results: </strong>Survivors identified three causes of social disconnection: (1) changes in self-concept and worldview, (2) symptom-related social withdrawal, and (3) unsupportive responses from others. The team developed and evaluated three intervention models, considering scope, effectiveness, resources, and barriers. An intervention including written materials, a website, a peer-led support group, and a social media forum, was prioritized as the most feasible and impactful option. A follow-up study will pilot-test the intervention to assess effects on wellbeing and work outcomes.</p><p><strong>Discussion: </strong>The team prioritized a multi-component intervention to foster connection and work engagement primarily targeting individual and interpersonal factors rather than workplace-level factors, likely reflecting the absence of a common employer. Findings highlight social connection as a modifiable target and support further intervention development and pilot-testing, with attention to accessibility and relevance across diverse survivor populations through cultural, economic, and structural adaptations.</p>","PeriodicalId":73061,"journal":{"name":"Frontiers in aging","volume":"7 ","pages":"1802482"},"PeriodicalIF":4.9,"publicationDate":"2026-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13350434/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148426913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of biopsychosocial frailty trends on survival and quality of life of older adults: a secondary analysis of data from a community-based active monitoring program.","authors":"Giuseppe Liotta, Olga Madaro, Clara Donnoli, Fabio Riccardi, Giulia Picardo, Fausto Ciccacci, Michele Bisogno, Paola Scarcella","doi":"10.3389/fragi.2026.1791524","DOIUrl":"10.3389/fragi.2026.1791524","url":null,"abstract":"<p><strong>Background: </strong>Advancing age frequently brings about a complex condition known as biopsychosocial frailty, which significantly impacts an older adult's survival and quality of life. This research investigates how changes in frailty levels affect mortality, hospitalization, and institutionalization, utilizing data from the \"Long Live the Elderly!\" program, a community-based initiative focused on proactive monitoring.</p><p><strong>Methods: </strong>A secondary analysis was conducted on data from 6,802 older adults participating in the LLE program across six Italian cities. Frailty was assessed using the Short Functional Geriatric Evaluation, which encompasses physical, psychological, and socio-economic dimensions. Trends in frailty were analyzed over an average follow-up period of 4.6 years, with survival outcomes evaluated using Cox proportional hazard models.</p><p><strong>Results: </strong>At baseline, 40.0% of participants were robust, 25.9% pre-frail, 27.4% frail, and 6.7% very frail. Frailty levels deteriorated in 36.9% of participants, while 11.2% experienced improvement. Higher frailty levels were significantly associated with increased mortality, hospitalization, and institutionalization. However, individuals whose frailty remained stable or improved showed significantly lower mortality rates compared to those whose frailty declined. Socio-economic enhancements were linked to better frailty outcomes, while psychophysical deterioration was the primary driver of declines.</p><p><strong>Conclusion: </strong>Frailty is a dynamic condition that may improve or worsen over time. Stabilizing or improving frailty trajectories was associated with reduced mortality, hospitalization, and institutionalization, supporting the relevance of multidimensional frailty monitoring in community settings These findings can support the importance of proactive multidimensional frailty monitoring in aging populations.</p>","PeriodicalId":73061,"journal":{"name":"Frontiers in aging","volume":"7 ","pages":"1791524"},"PeriodicalIF":4.9,"publicationDate":"2026-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13350052/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148426928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Age-associated B-cells across the rheumatoid arthritis continuum: from early immunopathogenesis to comorbidities.","authors":"Daniel Miranda-Prieto, Ana Suárez, Javier Rodríguez-Carrio","doi":"10.3389/fragi.2026.1812225","DOIUrl":"10.3389/fragi.2026.1812225","url":null,"abstract":"<p><p>Age-associated B cells (ABCs) are a B-cell subset with distinct transcription and functional properties. Their functions include antibodies secretion, cytokine production, antigen presentation and T-cell stimulation. ABCs have been found expanded in aging, infections and autoimmune diseases such as systemic lupus erythematous, multiple sclerosis and rheumatoid arthritis (RA). ABCs have emerged as plausible mediators of autoimmunity by virtue of their ability to produce autoantibodies and proinflammatory cytokines, as well as trigger T-cell activation, although mechanisms may differ across diseases. Moreover, ABCs may represent a mechanistic link between immunosenescence, premature aging and disease outcomes. Herein, we describe the current knowledge of ABCs in RA with a special focus in the early stages and comorbidity development. Accumulating evidence from preclinical and clinical studies with RA patients have demonstrated disturbances within the ABCs pool. Animal models suggest that ABCs play an important role already in the early phases of the disease and data from RA patients seem to support this hypothesis. Besides, RA risk factors and disease activity may be linked to ABCs expansion, which is associated with high levels of proinflammatory cytokines and correlated with skewed helper T-cell profiles, potentially contributing to inflammaging. Moreover, ABCs may not only be involved in the RA immunopathology, but also in the clinical expression of this disease at synovial and systemic levels. Potential roles of ABCs in cardiovascular, lung, neurological, kidney and metabolic comorbidities are identified, although level of evidence is heterogeneous and limited in some cases. Future perspectives for research, clinical translation and therapeutic implications are discussed.</p>","PeriodicalId":73061,"journal":{"name":"Frontiers in aging","volume":"7 ","pages":"1812225"},"PeriodicalIF":4.9,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13346199/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148426915","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A multi-modal longevity protocol integrating lifestyle, supplements, and autologous pro-regenerative cell-conditioned media: a pilot study.","authors":"Esteban Ortega, Guenole Addor, Sonam Bhatia, Max Lewinsohn, Pierre-Edouard Sottas","doi":"10.3389/fragi.2026.1732426","DOIUrl":"10.3389/fragi.2026.1732426","url":null,"abstract":"<p><strong>Introduction: </strong>Biological aging is a modifiable process contributing to functional decline and chronic disease risk. Multi-modal interventions targeting aging hallmarks have shown promise, yet human data integrating lifestyle, supplementation, and regenerative therapies remain limited.</p><p><strong>Methods: </strong>This single-arm, open-label pilot trial in 16 healthy adults aged 46-72 (14 completers) tested a 17-week multi-modal program integrating lifestyle optimization, targeted supplementation, and two intravenous infusions of autologous pro-regenerative cell-derived conditioned media (APRC-CM). Trial registration: ClinicalTrials.gov, NCT07322224.</p><p><strong>Results: </strong>The intervention improved clinical biomarkers and reduced biological-age measures (PhenoAge and an epigenetic DNA-methylation clock) despite the cohort's already healthy baseline (chronological age 59.3 years; PhenoAge 55.5 years; epigenetic age 57.9 years), consistent with a net reversal of biological age rather than merely a correction of age acceleration. PhenoAge declined by 2.0 years (p = 0.014), reaching 5.8 years below chronological age; epigenetic age decreased by 2.7 years (p = 0.003), widening the gap to 4.1 years. Exploratory response analysis revealed heterogeneity, with a larger-response subgroup showing a mean epigenetic-age reduction of 5.1 years versus 0.2 years in a smaller/no-response subgroup. Among baseline biomarkers, serum iron strongly predicted response: lower iron correlated with greater epigenetic-age reduction (r = 0.64; p = 0.013), identifying baseline iron status as a candidate prognostic biomarker of response. No adverse events were reported.</p><p><strong>Discussion: </strong>Such reductions in health-optimized individuals are notable and may indicate a lowering below expected norms rather than solely a correction of age acceleration. The observed response heterogeneity, together with baseline iron metabolism as a potential predictor of response, is hypothesis-generating and warrants validation in larger, controlled trials, particularly as this open-label, single-arm pilot lacked a control or sham comparator.</p>","PeriodicalId":73061,"journal":{"name":"Frontiers in aging","volume":"7 ","pages":"1732426"},"PeriodicalIF":4.9,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13346225/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148426959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Group-based trajectory modeling of hemoglobin change rate and impact of haemoglobin concentration on cardiovascular outcome after endovascular aneurysm repair a risk prediction model for persistent postoperative hemoglobin decline.","authors":"Xiao Li, Xiang Yan, Qing Sheng Lu","doi":"10.3389/fragi.2026.1867588","DOIUrl":"10.3389/fragi.2026.1867588","url":null,"abstract":"<p><strong>Objective: </strong>While postoperative hemoglobin decline following Endovascular Aneurysm Repair (EVAR) is a well-known phenomenon, the specific factors driving persistent hemoglobin reduction remain unclear. This observational, retrospective study seeks to establish distinct trajectories of hemoglobin change rates within the first 7 days following Endovascular Aneurysm Repair (EVAR) and to analyze the factors influencing persistent post-operative hemoglobin decline as well as Hb decrease, defined as preoperative minus postoperative Hb (g dl ^-1), on postoperative cardiovascular events in EVAR patients.</p><p><strong>Methods: </strong>The study population consisted of all patients who underwent endovascular aneurysm repair (EVAR) for abdominal aortic aneurysm (AAA), totaling 1,995 individuals, between 1 June 2002, and 31 March 2024. Group-based trajectory modeling (GBTM) was utilized to categorize distinct patterns of hemoglobin changes over a 7-day period in patients following EVAR. Baseline clinical and demographic characteristics predictive of trajectory group membership were analyzed using univariate screening and two multivariate binary logistic regression. The development of the two risk prediction models for persistent postoperative hemoglobin decline in patients undergoing EVAR was undertaken using logistic regression. The corresponding nomograms were subsequently constructed. The study second endpoint was 30-day postoperative cardiovascular events, including. myocardial infarction, heart failure, arrhythmias, stroke, asymptomatic troponin-T release and cardiovascular death.</p><p><strong>Results: </strong>We identified two trajectory groups: ' The decrease surpasses 20%' (n = 251, 16.8%) and 'under 20%' (n = 1,528, 83.2%). After adjusting for potential confounders, these groups were significantly linked to clinical outcomes like age, PAD, aneurysm characteristics. Intraoperative factors such as operation duration, blood loss, and graft details also showed associations. A risk prediction model, visualized with a nomogram, included factors like age, PAD, a larger maximum AAA diameter, and Iliac artery aneurysm presenting with bilateral involvement, achieving an AUC of 0.733 (95% CI: 0.690-0.775). The model showed 70.0% sensitivity and 66.7% specificity, with a calibration chart confirming strong alignment between observed and predicted values, and a clinical decision curve highlighting its potential clinical utility.</p><p><strong>Conclusion: </strong>In conclusion, our study identified that older age, maximum diameter of abdominal aortic aneurysm, and Iliac artery aneurysm presenting with bilateral were associated with continued hemoglobin decline post-EVAR. A drop in hemoglobin concentration exceeding 20% after elective EVAR surgery strongly predicts cardiovascular events within 30 days.</p>","PeriodicalId":73061,"journal":{"name":"Frontiers in aging","volume":"7 ","pages":"1867588"},"PeriodicalIF":4.9,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13346044/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148426910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Establishment and efficacy validation of sex-age-specific diagnostic cutoffs for sarcopenia: targeting the decline inflection points of muscle health indicators in community-dwelling middle-aged and elderly.","authors":"Wenwen Zhao, Mingjie Meng, Nuoya Li, Yiheng Geng, Hangtian Yu, Jinjia Zhang, Min Zhang, Meijing Song, Rongying Wang","doi":"10.3389/fragi.2026.1792871","DOIUrl":"10.3389/fragi.2026.1792871","url":null,"abstract":"<p><strong>Background: </strong>Sarcopenia is an age-related condition, with existing international guidelines predominantly focusing on the elderly and lacking age-specific diagnostic criteria. This study aims to investigate the prevalence of sarcopenia among middle-aged and elderly individuals in the Community, establish reference standards for muscle health indicators stratifiedby gender and age, and analyse age-related patterns of change and the validity of diagnostic cut-offs.</p><p><strong>Methods: </strong>A cross-sectional design was employed. Between April and June 2025, 2, 631 subjects aged ≥35 years from a community in Shijiazhuang, China, were enrolled and divided into sex-specific subgroups: 35-49, 50-64, and ≥65 years. Muscle Index (SMI), grip strength, and gait speed were measured. Diagnosis was based on the AWGS 2019 criteria. Stratified cutoffs were established using the P20 method, decline inflection points analysed via LOESS, and efficacy validated through ROC curves.</p><p><strong>Results: </strong>Overall sarcopenia prevalence was 6.65% (8.44% in males, 4.75% in females), rising to 15.26% in the ≥65 age group. Muscle indicators exhibited non-linear age-related decline with sex-specific inflection points; P20 cut-off decreased with age. AUC values for all indicators exceeded 0.75 in both the 50-64 and ≥65 age groups, demonstrating sound diagnostic performance.</p><p><strong>Conclusion: </strong>This study established sex and age stratified diagnostic cut-offs for sarcopenia in community-dwelling middle-aged and elderly individuals, elucidated the decline characteristics of core muscle indicators, and provided evidence for stratified community screening and precise prevention and control. It aligns with the concept of lifelong muscle health management and offers theoretical support for age-specific interventions.</p>","PeriodicalId":73061,"journal":{"name":"Frontiers in aging","volume":"7 ","pages":"1792871"},"PeriodicalIF":4.9,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13346177/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148426930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}