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Purpose: To investigate whether there is a direct, age-independent association between telomere length and visual acuity decline in a large community-based cohort study.
Methods: Participants older than 40 with linked leukocyte telomere length (LTL) were enrolled in NHANES. LTL was assayed using qPCR from the participants' blood samples. Best corrected visual acuity (BCVA) of the better-seeing eye was analyzed, with visual impairment (VI) defined as the BCVA of 20/40 or worse. LTL was grouped into quartiles, and its association with BCVA and VI was evaluated after adjusting for covariates.
Results: Among the 4,480 enrolled participants, the weighted means of age, BCVA, and telomere length were 56.1 ± 11.9 years, 0.05 ± 0.08 logMAR, and 5,662 ± 36 base pairs, respectively. The proportion of VI was 2.6%. After adjusting for covariates including sex, ethnicity, education, family poverty income ratio, general health status, hypertension, diabetes, smoking, and body mass index, BCVA was significantly worse in participants with shorter LTL, with a significant trend ( = 0.002). However, after further adjusting for age, the association between LTL and BCVA was no longer significant, without a trend ( = 0.640). No significant association or trend between LTL and VI was found in the stepwise logistic model.
Conclusions: No age-independent association between LTL and BCVA was found. Our study indicates LTL may not serve as a biomarker for age-related visual acuity decline.
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http://dx.doi.org/10.1080/09286586.2024.2422349 | DOI Listing |
Exp Gerontol
September 2025
Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT, USA; Salk Institute for Biological Studies, La Jolla, CA, 92037, USA; Department of Molecular Biology, University of Utah, Salt Lake City, UT, USA; Department of Biochemistry, University of Utah, Salt Lake Ci
Aging is the greatest risk factor for cardiovascular diseases (CVD) and is characterized by inflammation, oxidative stress, and cellular senescence. Cellular senescence is a state of persistent cell cycle arrest triggered by stressors such as DNA damage and telomere attrition. Senescent endothelial cells (ECs) can impair vascular function and promote inflammation, thereby contributing to CVD progression.
View Article and Find Full Text PDFKardiologiia
September 2025
National Medical Research Center for Therapy and Preventive Medicine, Moscow.
Atrial fibrillation (AF) is the most common form of cardiac arrhythmia, the prevalence of which increases with age. Slowing down senescence is one of the urgent challenges of modern science. Therefore, it is important to identify individuals with markers of premature cellular senescence for further development of pharmacological agents capable of slowing it.
View Article and Find Full Text PDFChron Respir Dis
September 2025
Department of Pulmonology, II.Medical Clinic and Polyclinic, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Case presentationDescription of a patient with a progressive destructive lung disease resembling pleuroparenchymal fibroelastosis, liver cirrhosis and bone marrow changes. Genetic workup identified a rare heterozygous coding variant in the (telomerase reverse transcriptase) gene c.472 C>T; p.
View Article and Find Full Text PDFBiomed Pharmacother
September 2025
Department of Medical Genetics, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Polyploidy, a conserved mechanism involved in normal development and tissue homeostasis, plays a paradoxical role in cancer by facilitating both tumor progression and therapeutic vulnerability. Although polyploidization may confer survival advantages to cancer cells, its controlled induction could represent an effective anticancer strategy. Aurora B kinase, a critical regulator of mitosis, plays a pivotal role in ensuring chromosomal integrity and preventing polyploidy.
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