Evidence map›Paper›PMID 40994876›Full record

ArticleInternational journal of biochemistry and molecular biology2025

Paternal contributions to telomere reprogramming in fetal development.

Sadia Farrukh, Saeeda Baig, Rubina Hussain

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Article in International journal of biochemistry and molecular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

3 authors.

Sadia FarrukhDepartment of Biological and Biomedical Sciences, Aga Khan University Karachi, Pakistan.
Saeeda BaigDepartment of Biochemistry, Ziauddin University Karachi, Pakistan.
Rubina HussainDepartment of Gynaecology and Obstetrician, Ziauddin University and Hospitals Karachi, Pakistan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTelomere length, the markers of biological aging, can be influenced by risk factors that may lead to health issues like chronic non-communicable diseases. This study explored the paternal telomere length influenced by diseases like diabetes and hypertension with age and its association with newborn telomere length (TL) and the telomerase gene.

methodsIn this cross-sectional study, 204 father-newborn dyads were recruited. The qPCR was used for the quantification of TL (T/S ratio), and Sanger sequencing was done for telomerase (TERT) genotype identification. Statistical Package for Social Sciences (SPSS) and GraphPad Prism Software were used for data analysis. The Spearman correlation was used to find an association between father and newborn TL. The Kruskal-Wallis and Mann-Whitney test was used to find differences among disease groups and TL. The P<0.05 was considered statistically significant.

resultsA positive correlation (r=0.39) (P<0.0001) was seen among fathers and newborn TL. The mean TL (T/S ratio) was found to be longer in healthy fathers and their newborns (1.67±1.18, 2.36±1.39), whereas significantly shorter TL (1.41±0.98, 2.02±1.58) (P=0.000) was seen in fathers suffering from diseases. The healthy fathers and their newborns TL (2.94±0.72, 3.10±0.61) were seen longer in the 15-20 (yrs) age category. Moreover, newborns of fathers (41-45 yrs) with both diabetes and hypertension had significantly longer telomere length (3.20±2.92) compared to their fathers (1.15±1.65) (P=0.006). The TERT risk genotype AC (rs2736100) was the most prevalent among the newborn girls.

conclusionA positive association with shorter TL in newborns was found in fathers having chronic diseases such as diabetes and hypertension, highlighting the contribution of fathers in reprogramming newborns' telomere biology.

Indexed as

diabeteshypertensionreprogrammingtelomeraseTelomeretelomere length

Identifiers

PMID40994876
PMCPMC12455035

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.