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Cancer and exercise
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Tormod S. Nilsen, Pernille Hojman, Henning Wackerhage
Currently, there is little evidence to suggest whether this is caused by an effect of exercise on mutagenesis. However, as almost 2/3 of all cancers are caused by mutations whose frequency is determined primarily by the rate of cell proliferation, any exercise-induced change of cell proliferation may affect how likely it is that a cancer develops. Another cause of mutations is genomic instability which might be linked to telomere length. Telomeres are the caps at the ends of our chromosomes, and these become shorter each time a cell divides ultimately meaning cells become senescent and stop dividing. There are a few studies that suggest exercise training affects telomere length. For example, Puterman et al (2010) demonstrated that exercise might inhibit telomere shortening (41), and later Sjögren et al demonstrated that less sedentary behaviour was associated with telomere lengthening (42). However, causality between lower incidence of cancer and increased telomere length in exercisers remains to be established (43).
Introduction to Cancer
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
Enabling replicative immortality: Although the first three characteristics described above are important for a cell to proliferate despite normal signaling controls, cell culture experiments demonstrate that cells need to overcome senescence and develop the characteristic of replicative immortality in order to develop into a tumor. This is normally achieved through overexpression of the telomerase enzyme to maintain telomere length.
Vitamin C and Somatic Cell Reprogramming
Published in Qi Chen, Margreet C.M. Vissers, Cancer and Vitamin C, 2020
An important function of vitamin C treatment during reprogramming and in the maintenance of pluripotent stem cells is the prevention of senescence and aging in long-term in vitro cultures. Vitamin C treatment silences the Ink4/Arf locus in ESCs and iPSCs by increasing the activity of H3K36 demethylases [35,36], which has the potential to rejuvenate aged cells [4,98]. The regulation of telomere length and the expression of telomerase-related genes that regulate telomerase activity can also have a profound effect on cell aging. Vitamin C treatment of human iPSC- and ESC-derived cardiomyocytes (CMs) reverses aging phenotypes and maintains the multipotent potential of MSCs in vitro by increasing telomerase activity and the expression of genes encoding telomerase-related RNA and protein components that protect telomere stability [97,99].
First-trimester maternal renin-angiotensin-aldosterone system activation and the association with maternal telomere length after natural and IVF/ICSI conceived pregnancies: the Rotterdam periconception cohort
Published in Hypertension in Pregnancy, 2023
D. Aoulad Fares, R.E. Wiegel, A.J. Eggink, J.B.J. van Meurs, S.P. Willemsen, A.H.J. Danser, R.P.M. Steegers-Theunissen
TL is suggested to be a long-term biomarker of chronic oxidative stress, as it shows the cumulative burden of oxidative stress (23). Short telomeres and telomere dysfunction, independently of age have been linked to numerous age-related diseases. Large population-based studies identify that subjects with shorter telomeres were characterized by a significantly higher hazard ratio for all-cause mortality compared to those with higher TL (36). Recently, it has been hypothesized that periconceptional long-term exposure to excessive oxidative stress and inflammation accelerates maternal TL shortening, and thereby increasing the underlying risk of neural tube defects in offspring (21). In this manner, shorter maternal TL were also associated with an increased risk of having a child with a ventricular septal defect (22). As the vulnerability of telomeres for oxidative stress and inflammation is well known, the RAAS is suggested to contribute to the acceleration of TL shortening. RAAS contributes to the pathogenesis of several human diseases that have a clear association with accelerated TL shortening, including cardiovascular diseases, stroke, and diabetes (37). By this means, several studies confirmed that Ang II induces the shorting of TL, in particular accelerated the rate of telomere loss (>2-fold versus control) in a dose-dependent manner (17,18,38). This is consistent with our findings that a higher level of renin is associated with significant shorter TL due to excessive exposure to oxidative stress.
Markers of cellular senescence is associated with persistent pulmonary pathology after COVID-19 infection
Published in Infectious Diseases, 2022
Tove Lekva, Thor Ueland, Bente Halvorsen, Sarah Louise Murphy, Anne Ma Dyrhol-Riise, Anders Tveita, Ane-Kristine Finbråten, Alexander Mathiessen, Karl Erik Müller, Trond Mogens Aaløkken, Ole Henning Skjønsberg, Tøri Vigeland Lerum, Pål Aukrust, Tuva Børresdatter Dahl
Recently, Mahmoodpoor et al. [2] reported that older COVID-19 patients with shorter telomeres and low lymphocyte counts were at increased risk for post-COVID pulmonary fibrosis. Indeed, short telomeres may result in chromosomal instability and loss of cell viability by inducing replicative senescence and apoptosis. Pulmonary alveolar cells with telomere dysfunction induce pulmonary fibrosis in mice, suggesting that dysfunctional telomeres in lungs could promote loss of viability and increased fibrosis. As patients with severe COVID-19 have shorter telomere lengths [3] and higher levels of cellular senescence [4], we hypothesized that circulating levels of the telomere-associated senescence markers chitotriosidase (CHIT1), β-galactosidase, cathelicidin antimicrobial peptide and stathmin 1 (STMN1) [5] could be elevated in COVID-19 patients compared to controls, and thus serve as markers of pulmonary sequelae following hospitalization for COVID-19.
Correlation between telomere length and efficacy of oral and long-acting injectable antipsychotics on severity and cognitive impairment of schizophrenia
Published in International Journal of Psychiatry in Clinical Practice, 2022
Nisha Pippal, Sumita Halder, Shruti Srivastava, Rajarshi Kar, Rachna Gupta, Almeida Edelbert Anthonio
Schizophrenia has emerged as a severe and debilitating psychiatric disorder affecting 0.3–0.7% of the population worldwide without gender differences (Charlson et al. 2018). It has a constellation of symptoms, mainly positive symptoms, negative symptoms, and cognitive impairment (Owen et al. 2016). Schizophrenia has been considered as a syndrome of early senescence and telomere length has also been found to be altered in these patients. Telomeres in mammals comprise repeat DNA nucleotides (TTAGGG)n and specific proteins, which are located at the terminal part of chromosomes and they safeguard the DNA which they enclose. Telomeres serve a vital role in various functions, like preventing the chromosomes from sticking to each other and preventing chromosome ends from DNA damage, helping in the separation of the chromosome during cell division and providing structural integrity to the human genome (Yu et al. 2008; Lu et al. 2013). Recent researchers are focussing on linking abnormal telomere length with several pathological conditions like malignancy (Rizvi et al. 2014) and schizophrenia (Yu et al. 2008).