Review
Version 1
Preserved in Portico This version is not peer-reviewed
Telomere Length as a Biomarker of Smoking-Induced Cellular Damage
Version 1
: Received: 8 March 2024 / Approved: 8 March 2024 / Online: 10 March 2024 (16:55:38 CET)
How to cite: Odah, M. Telomere Length as a Biomarker of Smoking-Induced Cellular Damage. Preprints 2024, 2024030545. https://doi.org/10.20944/preprints202403.0545.v1 Odah, M. Telomere Length as a Biomarker of Smoking-Induced Cellular Damage. Preprints 2024, 2024030545. https://doi.org/10.20944/preprints202403.0545.v1
Abstract
Smoking is a pervasive global health concern associated with a myriad of diseases, but its impact on cellular aging, particularly in relation to telomeres, is increasingly recognized. Telomeres, protective caps at the ends of chromosomes, play a crucial role in maintaining genomic integrity. This review critically examines the existing evidence on the association between smoking and telomere atrophy, exploring the molecular mechanisms involved and the implications for accelerated aging and heightened disease risk. The comprehensive analysis encompasses both cross-sectional and longitudinal studies, elucidating potential gender and age disparities. Insights into the molecular pathways linking smoking to telomere shortening are discussed, along with the broader implications for public health. The review concludes by outlining potential interventions and suggesting future research directions in this critical area.
Keywords
Smoking; telomere atrophy; cellular aging; disease risk; molecular mechanisms; gender disparities; age disparities.
Subject
Biology and Life Sciences, Biochemistry and Molecular Biology
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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