{"title":"Cancer burden among adults aged 65 years and older in Asia, 1990-2023: a systematic analysis of the Global Burden of Disease Study 2023.","authors":"Tianjiao Zhou, Enhui Zhou, Wen Lu, Jianyin Zou, Jingyu Zhang, Chenyang Li, Hangdong Shen, Chen Xu, Ying Shen, Jianxiang Li, Huaming Zhu, Chuan Xu, Hongliang Yi, Shankai Yin, Weijun Huang","doi":"10.1038/s41514-026-00419-0","DOIUrl":"10.1038/s41514-026-00419-0","url":null,"abstract":"<p><p>Older adults bear a substantial and increasing share of the cancer burden in Asia, yet its temporal trends, geographical heterogeneity, and inequalities remain insufficiently characterised. Using estimates from the Global Burden of Disease Study 2023, we assessed cancer incidence, mortality, and disability-adjusted life-years (DALYs) among adults aged 65 years and older across 34 Asian countries from 1990 to 2023, and examined demographic and epidemiological drivers, variations by location, sociodemographic index, age, and sex, with projections to 2050. In 2023, this population experienced 4.59 million new cancer cases, 3.27 million deaths, and 57.49 million DALYs. East Asia had the highest burden, whereas South Asia had the lowest rates but the fastest increases in incidence and mortality. Lung cancer remained the leading cancer, and digestive system cancers accounted for the greatest system-level burden. Population growth and population aging were the main contributors to rising cases and deaths, while favourable epidemiological changes were observed only in East and Southeast Asia. By 2050, the age-standardised incidence rate is projected to reach 1146.25 per 100,000 in females and 1518.97 in males. These findings call for more equitable and age-responsive cancer prevention and care strategies across Asia.</p>","PeriodicalId":94160,"journal":{"name":"npj aging","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2026-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13547383/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148166260","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":"Targeting mitophagy for neuroprotection: mechanisms and therapeutic opportunities.","authors":"Jiahui Yang, Jianfeng Li, Xintong Hou, Yifei Zheng, Zeyu Zhao, Ting Zhou, Tongwei Jing, Jiming Kong, Guohui Zhang, Ying Guo","doi":"10.1038/s41514-026-00424-3","DOIUrl":"10.1038/s41514-026-00424-3","url":null,"abstract":"<p><p>Mitochondria are essential for neuronal energy production, cellular homeostasis, and overall neuronal function. Due to their high metabolic demands and limited regenerative capacity, neurons are particularly vulnerable to mitochondrial dysfunction, which leads to ATP depletion, excessive reactive oxygen species (ROS) production, and calcium imbalance-ultimately causing oxidative stress, metabolic disruption, and neuronal death. Mitophagy is a selective process that removes damaged mitochondria through the autophagy-lysosome pathway. As a key mechanism of mitochondrial quality control, mitophagy preserves energy production, limits oxidative damage, and maintains mitochondrial network integrity. This process is regulated by pathways such as PINK1-Parkin and receptor-mediated mechanisms involving BNIP3 and FUNDC1, all of which help sustain cellular health by preventing mitochondrial dysfunction. Impaired mitophagy is a common feature of several neurodegenerative diseases, including Alzheimer's, Parkinson's, amyotrophic lateral sclerosis (ALS), and Huntington's disease, exacerbating mitochondrial damage and neuronal stress. Emerging therapeutic strategies that target mitophagy-ranging from pharmacological agents and gene therapies to dietary interventions-show promise in restoring mitochondrial quality and protecting neurons from degeneration. Nevertheless, challenges remain in translating these findings into effective clinical treatments. Mitophagy represents a critical mechanism for preserving neuronal integrity and offers a compelling target for innovative therapies against neurodegenerative disorders.</p>","PeriodicalId":94160,"journal":{"name":"npj aging","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13542155/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148159743","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}
npj agingPub Date : 2026-06-02DOI: 10.1038/s41514-026-00423-4
Rong Hua, Aimin Yang, Chun Sing Lam, Yuanyuan Wang, Chenglong Li
{"title":"Peripheral immunosenescence biomarkers and longitudinal cognitive decline: a large population-based study.","authors":"Rong Hua, Aimin Yang, Chun Sing Lam, Yuanyuan Wang, Chenglong Li","doi":"10.1038/s41514-026-00423-4","DOIUrl":"10.1038/s41514-026-00423-4","url":null,"abstract":"<p><p>Peripheral immunosenescence has been increasingly implicated in dementia pathogenesis. However, the contributions of specific lymphocyte subsets to cognitive outcomes remain poorly defined, and evidence from large-scale longitudinal studies is scarce. We leveraged data from the US Health and Retirement Study (n = 7444; mean age: 67.7 ± 9.7 years). Our primary analysis calculated three ratio metrics to quantify T-cell immunosenescence: the CD4:CD8 ratio, CD4 + EMRA: Naïve and CD8 + EMRA: Naïve ratios. Their longitudinal associations with 6-year cognitive decline were evaluated by linear mixed model adjusted for multiple covariates. We found that a higher CD8 + EMRA: Naïve ratio was significantly associated with accelerated cognitive decline (-0.050 point/year per SD; 95% CI: -0.066 to -0.033, P < 0.001). A nonlinear association was observed for the CD4:CD8 ratio (P for nonlinearity = 0.033), with only an intermediate level (the third quartile) associated with a slower cognitive decline. No significant association was found for the CD4 + EMRA: Naïve ratio. This study reveals a compartmentalized pattern in the associations of immunosenescent metrics with cognitive aging. The findings indicate a specific detrimental pathway characterized by an elevated CD8 + EMRA:Naïve ratio, whereas balanced CD4:CD8 homeostasis may play a beneficial role.</p>","PeriodicalId":94160,"journal":{"name":"npj aging","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13534656/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148152817","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}
npj agingPub Date : 2026-05-30DOI: 10.1038/s41514-026-00406-5
C Ráez-Meseguer, C Navas-Enamorado, X Capó, A M Galmes-Panades, A Molina de la Llave, M Mendez-Varela, M Martinez-Calvo, A Bennasar-Arbos, A Sánchez-Polo, L Masmiquel, M Torrens-Mas, M Monjo, J M Ramis, M Gonzalez-Freire
{"title":"Author Correction: MicroRNA profiles in plasma-derived extracellular vesicles across the human lifespan.","authors":"C Ráez-Meseguer, C Navas-Enamorado, X Capó, A M Galmes-Panades, A Molina de la Llave, M Mendez-Varela, M Martinez-Calvo, A Bennasar-Arbos, A Sánchez-Polo, L Masmiquel, M Torrens-Mas, M Monjo, J M Ramis, M Gonzalez-Freire","doi":"10.1038/s41514-026-00406-5","DOIUrl":"10.1038/s41514-026-00406-5","url":null,"abstract":"","PeriodicalId":94160,"journal":{"name":"npj aging","volume":"12 1","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13222346/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148102455","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}
npj agingPub Date : 2026-05-29DOI: 10.1038/s41514-026-00415-4
Raquel González-Martos, Irene Rodríguez-Gómez, Javier Galeano, Ignacio Ara, Luis M Alegre, Leocadio Rodríguez-Mañas, Francisco J Garcia-Garcia, Carmen Ramírez-Castillejo, Amelia Guadalupe-Grau
{"title":"Latent biochemical phenotypes delineate divergent health trajectories in older adults.","authors":"Raquel González-Martos, Irene Rodríguez-Gómez, Javier Galeano, Ignacio Ara, Luis M Alegre, Leocadio Rodríguez-Mañas, Francisco J Garcia-Garcia, Carmen Ramírez-Castillejo, Amelia Guadalupe-Grau","doi":"10.1038/s41514-026-00415-4","DOIUrl":"10.1038/s41514-026-00415-4","url":null,"abstract":"<p><p>Ageing heterogeneity hampers prevention and care. We used routine biochemical panels and unsupervised learning to identify latent phenotypes in community-dwelling older adults. In 1491 participants from the Toledo Study for Healthy Ageing (TSHA) with ~10-11 years of follow-up, 39 blood biomarkers were dimension-reduced and clustered, yielding three phenotypes: Healthy, Metabolic (subclinical dysmetabolism), and Haematological (low erythroid/renal profile). Phenotypes differed in functional capacity, frailty, and independence at baseline (all p < 0.05 after age/sex adjustment) and predicted long-term mortality (Metabolic women HR = 1.49, p = 0.016). Sex-specific analyses revealed distinct disease-trajectory patterns (e.g., hypertension in Metabolic women HR = 1.30, p = 0.005; thrombosis in Haematological men HR = 7.20, p = 0.018; syncope in Haematological women HR = 1.88, p = 0.009). Findings are partially replicated in a cohort of physically active older adults (EXERNET), supporting the generalizability of the Metabolic phenotype. Standard laboratory data, integrated through machine learning, capture ageing-relevant biology and stratify future risk without specialised assays, enabling low-cost, scalable precision prevention.</p>","PeriodicalId":94160,"journal":{"name":"npj aging","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2026-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13503819/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148059227","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}
npj agingPub Date : 2026-05-29DOI: 10.1038/s41514-026-00409-2
Rachel Upthegrove, Amalie C M Couch, Antonio de Marvao, Benjamin I Perry, Fabiana Corsi-Zuelli, Jack Rogers, Lahiru Handunnetthi, Nicholas M Barnes, Nikolaos Koutsouleris, Paris A Lalousis, Toby Pillinger, Zachary Freyberg
{"title":"Psychosis as a multisystem disorder of aberrant aging.","authors":"Rachel Upthegrove, Amalie C M Couch, Antonio de Marvao, Benjamin I Perry, Fabiana Corsi-Zuelli, Jack Rogers, Lahiru Handunnetthi, Nicholas M Barnes, Nikolaos Koutsouleris, Paris A Lalousis, Toby Pillinger, Zachary Freyberg","doi":"10.1038/s41514-026-00409-2","DOIUrl":"10.1038/s41514-026-00409-2","url":null,"abstract":"<p><p>Psychotic disorders, including schizophrenia and affective psychosis, affect ~3% of the population and typically emerge in early adulthood. Cardiometabolic disease accounts for much of the 20-year life-expectancy gap in psychosis. Evidence indicates potentially causal processes, often seen in aging, act within and beyond the brain, and before the onset of treatment; these include inflammation, metabolic and mitochondrial dysfunction. Here we synthesize evidence and propose a framework that proposes psychosis as a multisystem disorder of accelerated aging, and outline implications for aging-targeted interventions.</p>","PeriodicalId":94160,"journal":{"name":"npj aging","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2026-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13507340/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148059188","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}
npj agingPub Date : 2026-05-28DOI: 10.1038/s41514-026-00422-5
Jhommara Bautista, Andrés López-Cortés
{"title":"Mitochondrial drivers of stem cell aging and inflammaging.","authors":"Jhommara Bautista, Andrés López-Cortés","doi":"10.1038/s41514-026-00422-5","DOIUrl":"10.1038/s41514-026-00422-5","url":null,"abstract":"<p><p>Mitochondria are increasingly recognized as master regulators of aging, integrating bioenergetics, redox control, stem cell fate, and innate immune signaling. This review synthesizes evidence that mitochondrial dysfunction is not only a hallmark but also an upstream driver of stem cell exhaustion and inflammaging. We discuss how age-associated mitochondrial DNA (mtDNA) mutations and clonal mosaicism impair respiration and reshape metabolite availability, thereby reprogramming long-lived epigenetic states that govern quiescence, lineage commitment, and regenerative output. In parallel, erosion of mitochondrial quality control (MQC), including fission-fusion balance, mitophagy, and the mitochondrial unfolded protein response (UPRmt), permits the persistence of reactive oxygen species (ROS)-producing organelles and lowers containment of mitochondrial danger signals. A central advance is that mitochondrial damage can be decoded as inflammation: cytosolic mtDNA and other mitochondrial damage-associated molecular patterns (mtDAMPs) activate cGAS-STING and NF-κB pathways, reinforcing senescence-linked cytokine circuits and chronic inflammatory tone. We further highlight nicotinamide adenine dinucleotide (NAD⁺) depletion as a metabolic bottleneck that compromises sirtuin-dependent resilience and can enforce mitochondrial dysfunction-associated senescence (MiDAS), linking redox collapse to altered senescence phenotypes and regenerative decline. Finally, we evaluate emerging mitochondria-targeted rejuvenation strategies, NAD⁺ repletion, mitophagy enhancers, mitochondrial transplantation/engineering, and precision elimination of mutant mtDNA using mitochondria-targeted transcription activator-like effector nucleases (mitoTALENs) or zinc-finger nucleases (mitoZFNs), emphasizing tissue-specific thresholds and context dependence for effective healthspan extension.</p>","PeriodicalId":94160,"journal":{"name":"npj aging","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2026-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13500825/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148059203","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}
npj agingPub Date : 2026-05-28DOI: 10.1038/s41514-026-00401-w
Martin R Späth, Sita Arjune, Katrin Bohl, Markus M Rinschen, Christine S Falk, Philipp Antczak, Franziska Grundmann, Torsten Kubacki, K Johanna R Hoyer-Allo, Michael Ignarski, Felix C Koehler, Kathrin Kaufmann, Malte P Bartram, Tristan Wagner, Michael Thomas, Jan Wilm Lackmann, Adam Wahida, Christoph Schmaderer, Stephan Kemmner, Christine E Kurschat, Thomas Benzing, Dirk Stippel, Volker Burst, Roman-Ulrich Müller
{"title":"An in-depth analysis of the molecular changes induced by short-term calorie restriction before living kidney donation.","authors":"Martin R Späth, Sita Arjune, Katrin Bohl, Markus M Rinschen, Christine S Falk, Philipp Antczak, Franziska Grundmann, Torsten Kubacki, K Johanna R Hoyer-Allo, Michael Ignarski, Felix C Koehler, Kathrin Kaufmann, Malte P Bartram, Tristan Wagner, Michael Thomas, Jan Wilm Lackmann, Adam Wahida, Christoph Schmaderer, Stephan Kemmner, Christine E Kurschat, Thomas Benzing, Dirk Stippel, Volker Burst, Roman-Ulrich Müller","doi":"10.1038/s41514-026-00401-w","DOIUrl":"10.1038/s41514-026-00401-w","url":null,"abstract":"<p><p>Aging reduces cellular resilience and increases susceptibility to organ injury, notably acute kidney injury (AKI). Ischemia-reperfusion injury (IRI) influences outcomes after kidney transplantation. In animal models, short-term calorie restriction (CR) extends lifespan and protects kidneys from IRI, but translation to patients is limited due to incomplete mechanistic insight. This study examined clinical and molecular effects of short-term CR in living kidney donors. Twelve donors were alternately assigned to CR or an ad libitum diet. CR participants consumed a formula diet providing 50% of individual caloric needs for seven days before donation. Clinical parameters and biosamples from perirenal fat, renal arteries, ureters, kidney biopsies, blood, and urine were collected. Primary outcomes were CR-induced molecular changes; clinical outcomes were secondary. CR was well tolerated and caused significant weight loss without affecting AKI incidence or increasing adverse events. Lipidomic and proteomic analyses showed enhanced lipolysis and proteostasis, reduced insulin signaling, sex-specific effects, and decreased inflammatory factors in donor arteries and ureter tissue. This hypothesis-generating study indicates that short-term CR before donation is feasible and suggests that CR promotes organ protection in humans by dampening insulin signaling and inflammation, providing a basis for future targeted interventions in clinical and transplant research moving forward.</p>","PeriodicalId":94160,"journal":{"name":"npj aging","volume":"12 1","pages":""},"PeriodicalIF":13.0,"publicationDate":"2026-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13219448/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148059254","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}
npj agingPub Date : 2026-05-26DOI: 10.1038/s41514-026-00414-5
Beatriz Escobar-Doncel, Xiaoyi Zhang, Åsne Ljøstad, Mario Fernández de la Puebla, Shreyas Balachandra Rao, Synnøve Algrøy Fjeldstad, Maja Tvedt Dahle, Mahmood Amiry-Moghaddam, Magnar Bjørås, Evandro Fei Fang, Wannan Tang
{"title":"Two-photon in vivo imaging reveals cell type-specific mitophagy dynamic changes in mouse somatosensory cortex during aging.","authors":"Beatriz Escobar-Doncel, Xiaoyi Zhang, Åsne Ljøstad, Mario Fernández de la Puebla, Shreyas Balachandra Rao, Synnøve Algrøy Fjeldstad, Maja Tvedt Dahle, Mahmood Amiry-Moghaddam, Magnar Bjørås, Evandro Fei Fang, Wannan Tang","doi":"10.1038/s41514-026-00414-5","DOIUrl":"10.1038/s41514-026-00414-5","url":null,"abstract":"<p><p>Mitochondrial homeostasis is majorly maintained through mitochondrial autophagy (mitophagy). Recent research highlights the region- and cell type-specific nature of mitophagy during brain aging; however, these dynamics have largely remained unexplored in living brains. To address this gap, we conducted two-photon mt-Keima imaging in somatosensory cortical neurons and astrocytes in behaving male mice across two age groups, including 2-3-month-old (early-aged) and 18-20-month-old (old-aged) mice. We show reduced mitophagy in both cell types during aging, and we consistently found a higher level of mitophagy in astrocytes compared to neurons at the same age, in both age groups. Pharmacological augmentation of NAD<sup>+</sup>, a pivotal metabolite that induces mitophagy but normally declines in the aging brain, increased cellular mitophagy in both neurons and astrocytes in old-aged male mice at the dose and method of administration tested. Collectively, our data support an age-dependent reduction of mitophagy in neurons and astrocytes, at least in mouse somatosensory cortex, while NAD<sup>+</sup> repletion offsets such reduction.</p>","PeriodicalId":94160,"journal":{"name":"npj aging","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2026-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13490384/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148038814","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}
npj agingPub Date : 2026-05-25DOI: 10.1038/s41514-026-00417-2
Qinghong Li, Linxing Yao
{"title":"Evaluation of equation as a classifier for kidney function in domestic cats: a proof-of-concept study.","authors":"Qinghong Li, Linxing Yao","doi":"10.1038/s41514-026-00417-2","DOIUrl":"10.1038/s41514-026-00417-2","url":null,"abstract":"<p><p>In human medicine, estimated glomerular filtration rate (eGFR) is routinely used to assess renal function. In cats, reliable eGFR formulas are not yet available. To test the hypothesis that a human eGFR equation with four metabolites can effectively distinguish cats with different renal functions, two cohorts of cats were retrospectively enrolled. Cohort 1 included 34 colony cats and cohort 2 had 29 client-owned cats. The metabolite markers were quantified in cat serum and renal function was estimated using the adapted equation (eRF<sub>fel</sub>). Receiver Operating Characteristic Area Under the Curve for eRF<sub>fel</sub> as a binary classifier were 0.9714 and 0.9958, and 0.9731 and 0.9643 as a ternary classifier for cohort 1 and cohort 2, respectively. In cohort 1, eRF<sub>fel</sub> was 1.30 ± 0.04 (Mean ± SEM, mL/min/kg), 0.78 ± 0.06, and 0.36 ± 0.05 for healthy control, IRIS Chronic Kidney Disease (CKD) stages 1 and 2 (CKD1/2), and stages 3 and 4 (CKD3/4), respectively, and 1.30 ± 0.06, 0.72 ± 0.05, and 0.47 ± 0.04 for healthy control, CKD stage 2, and CKD stage 3 in cohort 2, respectively (both P < 0.0001). Although the original equation was trained on human data, eRF<sub>fel</sub> was associated positively with urine specific gravity, but negatively with serum symmetric dimethylarginine and creatinine in cats (all P < 0.0001). The preliminary results demonstrated the effectiveness of eRF<sub>fel</sub> as a classifier for feline renal function.</p>","PeriodicalId":94160,"journal":{"name":"npj aging","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2026-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13578686/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148019795","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}