Iron Toxicity and Hypothalamic Dysfunction: The Central Role of Kisspeptin Signaling in Thalassemia Associated Delayed Puberty

Authors

  • Laila M Sherief, Mervat Atfy , Ihab Abdelhameed, Doaa Metwaly , Esraa Hassan Ibrahim Elsayed
  • 10.48047/pegegog.2024.14.3.96

Keywords:

B-thalassemia; iron overload; hypothalamic dysfunction; kisspeptin; KISS1; KISS1R; delayed puberty; hypogonadotropic hypogonadism; oxidative stress; neuroendocrinology

Abstract

Background: Delayed puberty is among the most prevalent endocrine complications in transfusion-dependent βthalassemia, primarily resulting from chronic iron overload and its toxic effects on the hypothalamic–pituitary–gonadal axis. While pituitary dysfunction has historically

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References

Moos T, Morgan EH. The metabolism of neuronal iron and its pathogenic role in neurological disease. Ann N Y Acad Sci. 2004;1012:14-26.

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Published

2024-06-24

How to Cite

Laila M Sherief, Mervat Atfy , Ihab Abdelhameed, Doaa Metwaly , Esraa Hassan Ibrahim Elsayed, & 10.48047/pegegog.2024.14.3.96. (2024). Iron Toxicity and Hypothalamic Dysfunction: The Central Role of Kisspeptin Signaling in Thalassemia Associated Delayed Puberty . Pegem Journal of Education and Instruction, 14(3), 992–1000. Retrieved from https://www.pegegog.net/index.php/pegegog/article/view/4962

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