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Review

The Hypothesis of the Prolonged Cell Cycle in Turner Syndrome

1
Biological Sciences School, Faculty of Biological Sciences, Central University of Ecuador, Quito 170113, Ecuador
2
Genetic Research Institute, University of Zulia, Maracaibo 4001, Venezuela
*
Author to whom correspondence should be addressed.
Academic Editors: Julia Thom Oxford and Makenna Hardy
J. Dev. Biol. 2022, 10(2), 16; https://doi.org/10.3390/jdb10020016
Received: 28 February 2022 / Accepted: 13 March 2022 / Published: 11 May 2022
(This article belongs to the Special Issue Advances in Development: Focus on Rare Congenital Diseases)
Turner syndrome (TS) is a chromosomal disorder that is caused by a missing or structurally abnormal second sex chromosome. Subjects with TS are at an increased risk of developing intrauterine growth retardation, low birth weight, short stature, congenital heart diseases, infertility, obesity, dyslipidemia, hypertension, insulin resistance, type 2 diabetes mellitus, metabolic syndrome, and cardiovascular diseases (stroke and myocardial infarction). The underlying pathogenetic mechanism of TS is unknown. The assumption that X chromosome-linked gene haploinsufficiency is associated with the TS phenotype is questioned since such genes have not been identified. Thus, other pathogenic mechanisms have been suggested to explain this phenotype. Morphogenesis encompasses a series of events that includes cell division, the production of migratory precursors and their progeny, differentiation, programmed cell death, and integration into organs and systems. The precise control of the growth and differentiation of cells is essential for normal development. The cell cycle frequency and the number of proliferating cells are essential in cell growth. 45,X cells have a failure to proliferate at a normal rate, leading to a decreased cell number in a given tissue during organogenesis. A convergence of data indicates an association between a prolonged cell cycle and the phenotypical features in Turner syndrome. This review aims to examine old and new findings concerning the relationship between a prolonged cell cycle and TS phenotype. These studies reveal a diversity of phenotypic features in TS that could be explained by reduced cell proliferation. The implications of this hypothesis for our understanding of the TS phenotype and its pathogenesis are discussed. It is not surprising that 45,X monosomy leads to cellular growth pathway dysregulation with profound deleterious effects on both embryonic and later stages of development. The prolonged cell cycle could represent the beginning of the pathogenesis of TS, leading to a series of phenotypic consequences in embryonic/fetal, neonatal, pediatric, adolescence, and adulthood life. View Full-Text
Keywords: cell proliferation; congenital heart disease; embryonic lethality; folliculogenesis; neuropsychological profile; prolonged cell cycle; short stature; Turner syndrome cell proliferation; congenital heart disease; embryonic lethality; folliculogenesis; neuropsychological profile; prolonged cell cycle; short stature; Turner syndrome
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MDPI and ACS Style

Álvarez-Nava, F.; Soto-Quintana, M. The Hypothesis of the Prolonged Cell Cycle in Turner Syndrome. J. Dev. Biol. 2022, 10, 16. https://doi.org/10.3390/jdb10020016

AMA Style

Álvarez-Nava F, Soto-Quintana M. The Hypothesis of the Prolonged Cell Cycle in Turner Syndrome. Journal of Developmental Biology. 2022; 10(2):16. https://doi.org/10.3390/jdb10020016

Chicago/Turabian Style

Álvarez-Nava, Francisco, and Marisol Soto-Quintana. 2022. "The Hypothesis of the Prolonged Cell Cycle in Turner Syndrome" Journal of Developmental Biology 10, no. 2: 16. https://doi.org/10.3390/jdb10020016

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