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Current Stem Cell Research & Therapy

Editor-in-Chief

ISSN (Print): 1574-888X
ISSN (Online): 2212-3946

Review Article

Enhancing Spermatogenesis in Non-obstructive Azoospermia Through Mesenchymal Stem Cell Therapy

Author(s): Ria Margiana*

Volume 19, Issue 11, 2024

Published on: 12 January, 2024

Page: [1429 - 1441] Pages: 13

DOI: 10.2174/011574888X283311231226081845

Price: $65

Abstract

Stem cells hold great promise as novel and encouraging therapeutic tools in the treatment of degenerative disorders due to their differentiation potential while maintaining the capability to self-renewal and their unlimited ability to divide and regenerate tissue. A variety of different types of stem cells can be used in cell therapy. Among these, mesenchymal stem cell (MSC) therapy has gradually established itself as a novel method for treating damaged tissues that need restoration and renewal. Male infertility is an important health challenge affecting approximately 8-12% of people around the world. This abnormality can be caused by primary, congenital, acquired, or idiopathic reasons. Men with no sperm in their semen have a condition called azoospermia, caused by non-obstructive (NOA) causes and post-testicular obstructive causes. Accumulating evidence has shown that various types of MSCs can differentiate into germ cells and improve spermatogenesis in the seminiferous tubules of animal models. In addition, recent studies in animal models have exhibited that extracellular vesicles derived from MSCs can stimulate the progression of spermatogenesis and germ cell regeneration in the recipient testes. In spite of the fact that various improvements have been made in the treatment of azoospermia disorder in animal models by MSC or their extracellular vesicles, no clinical trials have been carried out to test their therapeutic effect on the NOA. In this review, we summarize the potential of MSC transplantation for treating infertility caused by NOA.

Keywords: MSCs, azoospermia, stem cell therapy, male infertility, spermatogenesis, NOA.


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