What does the research say about telomere length?
Telomeres are repetitive DNA-protein structures that cap chromosome ends. Research has examined telomere length as a biomarker of cellular aging, with studies exploring telomerase activation, epigenetic reprogramming, an
Telomeres are repetitive nucleotide sequences (TTAGGG in vertebrates) bound by shelterin proteins that protect chromosome ends from degradation and fusion. Telomere length (TL) is considered a biomarker of cellular aging; progressive shortening occurs with each cell division and is influenced by oxidative stress and inflammation [9]. In human cell lines, the tetrapeptide Epitalon has been reported to increase telomere length through telomerase upregulation or alternative lengthening of telomeres (ALT) activity [4][5].
Research on telomere length centres on the telomerase reverse transcriptase (TERT) pathway and its regulation, as well as on ALT mechanisms. Telomerase enzyme activity and hTERT mRNA expression are key molecular readouts in studies of telomere maintenance [4][5].
Research Studies
Epitalon and telomerase upregulation in human cell lines
Epitalon, a naturally occurring tetrapeptide, has been studied for its effects on telomere length in human cell lines. The compound is reported to induce telomerase enzyme activity, leading to telomere extension. Quantitative data on the biomolecular pathway, including hTERT mRNA expression, telomerase enzyme activity, and ALT activation, have been generated in these in vitro models [4][5]. A correction to one of these studies has been published [3].
Transient reprogramming and endothelial cell aging
In senescent endothelial cells (ECs), non-genetic overexpression of Yamanaka factors induced partial functional rejuvenation and attenuation of senescence-associated features. This was demonstrated in vitro through gene expression quantification and cellular function measurements, and further in vivo experiments were performed in a hind-limb model [1]. Telomere length was not the primary endpoint, but the study highlights cellular reprogramming as a strategy to counteract aging phenotypes.
Collagen peptides and telomere length in overweight adults
A clinical trial is investigating whether daily collagen peptide supplementation can stabilize or lengthen telomeres and improve related markers of cellular aging in adults aged 50–70 years with overweight and low-to-moderate physical activity. The study aims to determine if six months of collagen peptides stabilizes or extends telomere length and increases telomerase activity compared with placebo, and whether any changes are associated with lower inflammation, healthier body composition, and better functional health [2].
Nicotinamide mononucleotide (NMN) and immunosenescence
A placebo-controlled clinical trial is examining the effect of nicotinamide mononucleotide (NMN) supplementation on immunosenescence in middle-aged and elderly individuals with metabolic disorders. The study focuses on glucose and lipid metabolism and immune system aging, but telomere length is not specified as an outcome [6].
Metformin and molecular aging in prediabetes
Metformin has been shown to prevent progression of prediabetes to overt diabetes and to improve lifespan in animal models through an anti-ageing pathway driven by mTOR. In the context of molecular aging, a clinical trial is investigating metformin's effects in Asian Indians with prediabetes, a population with high incidence rates. Telomere length is among the molecular aging markers being assessed [7].
Kisspeptin-54 and chondrocyte senescence in osteoarthritis
Kisspeptin-54, a neuropeptide, was investigated for its role in chondrocyte senescence in osteoarthritis. The study reports that Kisspeptin-54 ameliorates chondrocyte senescence via SIRT3-mediated telomere protection and p53 acetylation inhibition. This work was conducted in in vitro and in vivo models of osteoarthritis [11].
Telomere length and mitochondrial DNA in porcine embryos
In parthenogenetically activated porcine embryos, the relationship between mitochondrial DNA copy number (mt-cn) and telomere length (TL) was investigated. Both are considered secondary markers of embryonic quality. The study used oocytes collected from gilt ovaries, matured and activated, to assess these parameters [8].
Telomere length in non-functional adrenal incidentalomas
Telomere length was measured in patients with non-functional adrenal incidentalomas. The study aimed to explore associations with metabolic syndrome components linked to cellular aging, considering genetic and environmental factors such as oxidative stress and inflammation [9].
Breast DNA methylation-based biological ageing and obesity-related risk
Epigenetic ageing measures, including DNA methylation-based estimates, were studied in relation to obesity-related breast cancer risk markers. The research focused on normal breast tissue and aimed to link biological ageing with breast cancer risk, though telomere length was not a direct measure [10].
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Sources
- [1] Functional rejuvenation of endothelial cell aging by transient reprogramming
- [2] Collagen Peptides and Cellular Aging
- [3] Correction: Epitalon increases telomere length in human cell lines through telomerase upregulation or ALT activity
- [4] Epitalon increases telomere length in human cell lines through telomerase upregulation or ALT activity
- [5] Epitalon increases telomere length in human cell lines through telomerase upregulation or ALT activity
- [6] The Impact of Nicotinamide Mononucleotide Sustained-release Tablets on Immunosenescence and Metablism in Middle-aged and Elderly Individuals With Metabolic Disorders
- [7] Metformin and Molecular Aging in Prediabetes
- [8] Telomere regulation of mitochondria in porcine parthenogenetic embryos
- [9] Telomere length in patients with non-functional adrenal incidentalomas
- [10] Associations of breast DNA methylation-based measures of biological ageing with obesity-related breast cancer risk markers
- [11] Kisspeptin-54 ameliorates chondrocyte senescence in osteoarthritis via SIRT3-mediated telomere protection and p53 acetylation inhibition