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Introduction: Although previous studies investigated the potential adverse effects of endocrine-disrupting chemicals (EDCs) on biological age acceleration and aging-related diseases, the mixed effect of multiple types of EDCs on biological age acceleration, including its potential underlying mechanism, remains unclear.
Methods: Data from the National Health and Nutrition Examination Survey (NHANES) were used to analyze biological age measures, including Klemera-Doubal method biological age (KDM-BA), phenotypic age, and homeostatic dysregulation (HD). Weight quantile sum (WQS) regression was performed to screen biological age-related EDCs (BA-EDCs) and assess the mixed effect of BA-EDCs on biological age acceleration and aging-related disease. Targets of BA-EDCs were obtained from three databases, while heart aging-related genes were obtained from the Aging Anno database. Protein-protein interaction (PPI) network and MCODE algorithm were applied to identify potential interactions between BA-EDC targets and heart aging-related genes. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis were performed to identify related pathways.
Results: This cross-sectional study included 1,439 participants. A decile increase in BA-EDCs co-exposure was associated with 0.31 years and 0.17 years of KDM-BA and phenotypic age acceleration, respectively. The mixed effect of BA-EDCs was associated with an increased prevalence of atherosclerotic cardiovascular disease (ASCVD). Vitamins C and E demonstrated a significant interaction effect on the association between BA-EDCs and KDM-BA acceleration. PPI network and functional enrichment analysis indicated that the AGE-RAGE signaling pathway in diabetic complications was significantly enriched.
Conclusion: Our results showed that the co-exposure effect of BA-EDCs was associated with biological age acceleration and ASCVD, with the AGE-RAGE signaling pathway being the underlying mechanism. Vitamins C and E may also be an actionable target for preventing EDC-induced biological aging.
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http://dx.doi.org/10.1016/j.envint.2024.108447 | DOI Listing |
Anat Sci Educ
September 2025
Human Anatomy, Vita-Salute San Raffaele University, Milan, Italy.
As emerging technologies reshape both the body and how we represent it, anatomical education stands at a threshold. Virtual dissection tools, AI-generated images, and immersive platforms are redefining how students learn anatomy, while real-world bodies are becoming hybridized through implants, neural interfaces, and bioengineered components. This Viewpoint explores what it means to teach human anatomy when the body is no longer entirely natural, and the image is no longer entirely real.
View Article and Find Full Text PDFAnn Surg Oncol
September 2025
Department of Thoracic Surgery, Clinical Oncology School of Fujian Medical University, Fujian Cancer Hospital, Fuzhou, Fujian Province, China.
Background: RUNX3 acts as a tumor suppressor gene in non-small-cell lung cancer (NSCLC), yet its specific biological mechanism is still unclear. This study aimed to uncover tumor microenvironment (TME) changes in NSCLC with varying RUNX3 expression statuses through single-cell RNA sequencing.
Patients And Methods: In total, seven patients with NSCLC with detailed pathological data were involved, with three both paracancerous and cancerous tissue samples.
Aging Cell
September 2025
School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, New South Wales, Australia.
Ageing is one of the most significant risk factors for heart disease; however, it is still not clear how the human heart changes with age. Taking advantage of a unique set of pre-mortem, cryopreserved, non-diseased human hearts, we performed omics analyses (transcriptomics, proteomics, metabolomics, and lipidomics), coupled with biologically informed computational modelling in younger (≤ 25 years old) and older hearts (≥ 50 years old) to describe the molecular landscape of human cardiac ageing. In older hearts, we observed a downregulation of proteins involved in calcium signalling and the contractile apparatus.
View Article and Find Full Text PDFJ Thromb Haemost
September 2025
Department of Immunology and Inflammation, Centre for Haematology, Imperial College, London, UK. Electronic address:
Background: The VWF Phe2561Tyr variant has been previously shown to exhibit gain-of-function like activity and increase the risk of repeated MI in patients below 55 years of age. It was hypothesised that altered stem dynamics enhanced the responsiveness of the molecule to shear stress. In this study we investigated the evolutionary significance of the amino acid at position 2561 and functional impacts of variants at this site.
View Article and Find Full Text PDFDiabetes Metab
September 2025
Paris Diabetology Federation, Paris, France; Institut Necker Enfants Malades, INSERM U1151, CNRS UMR 8253, IMMEDIAB Laboratory, Université Paris Cité, Paris, France; Department of Diabetology and Endocrinology, Bichat Hospital, AP-HP, Paris, France.
Aim: - To investigate the incidences of death and lower limb amputation (LLA) among patients hospitalized with a first diabetic foot ulcer and to identify the associated risk factors.
Methods: - We leveraged medical records from 08/2017 to 10/2023 in the clinical data warehouse of the Greater Paris Hospitals. The primary outcome was the cumulative incidence of death estimated at 12 months.