Telomerase activation in the treatment of aging or degenerative diseases: a systematic review
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Telomerase activation in the treatment of aging or degenerative diseases: a systematic review P. Prieto‑Oliveira1 Received: 11 July 2020 / Accepted: 24 September 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Telomeres are protective structures that are shortened during the lifetime, resulting in aging and degenerative diseases. Subjects experiencing aging and degenerative disorders present smaller telomeres than young and healthy ones. The size of these structures can be stabilized by telomerase, an enzyme which is inactive in adult tissues but functional in fetal and newborn tissues and adult testes and ovaries. The aim of this study was to perform a systematic review to evaluate the effect of telomerase activation in the treatment of degenerative and aging disorders. We accomplished the search using the Pubmed interface for papers published from September 1985 to April 16th, 2020. We found twenty one studies that matched our eligibility criteria. I concluded that telomerase is probably a potential and safe treatment for aging and degenerative diseases, demonstrating neither side effects nor risk of cancer in the selected studies. Further studies in humans are needed to confirm safety and efficiency of this treatment. Keywords Telomere · Telomerase · Aging · Enzyme activation · Biological therapy · Systematic review
Introduction Telomeres are highly conserved repetitive DNA sequences (TTAGGG)n, located at the ends of chromosomes, and are responsible for maintenance of genome stability [1]. These protective structures are progressively shortened during each round of DNA replication. When they reach a critical length, apoptosis or senescence may occur, depending on the cell type, due to the activation of p53 tumor suppressor protein. This DNA damage response results in aging and degenerative diseases [2]. Various studies indicate that patients exhibiting disorders as stroke [3, 4], atherosclerosis [5], hypertension [6, 7], dyskeratosis congenita [8], pulmonary fibrosis [9–11], chronic obstructive pulmonary disease [12], schizophrenia [13–17], Alzheimer disease [18], amyotrophic lateral sclerosis [19], organs failure [20], aplastic anemia [11, 21, * P. Prieto‑Oliveira [email protected] 1
Laboratory of Retrovirology, Department of Microbiology, Immunology and Parasitology, Federal University of São Paulo, Pedro de Toledo Street 781, 16th Floor, Retrovirology, Vila Clementino, São Paulo, SP CEP: 04039‑032, Brazil
22], osteoporosis [23, 24], type 2 diabetes mellitus [25–27], chronic renal disease [28], age-related macular degeneration [29], Huntington’s syndrome [30], rheumatoid arthritis [31, 32], and cirrhosis [33, 34] present smaller telomeres compared to healthy ones. Fetuses, newborns and adult testes and ovaries are able to stabilize the size of telomeres by means of telomerase activity. However, telomerase is inactive in mature spermatozoa and oocytes, and in somatic cells from the neonatal period onward [35]. Telomerase is a DNA polymerase responsible for
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