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This review highlights hypogonadism's impact on Leydig cell function, suggesting that noncoding RNA may offer new insights into infertility mechanisms.
The study of male reproductive function is a critical area that requires an in-depth understanding of the underlying regulatory mechanisms. Male fertility has become a growing global health concern, driven by the increasing prevalence of hypogonadism and associated infertility. The existing treatment options for reproductive diseases have not achieved complete success, which highlights the need to explore novel therapeutic approaches. The malfunction and/or suppression of molecular regulators involved in the maintaining of cellular homeostasis under stress conditions have been identified as a key issue in Leydig cell insufficiency. miRNAs are noncoding RNA molecules that play a pivotal function in regulating gene expression and are implicated in diverse physiological and pathological conditions. In recent years, investigation into noncoding RNA-mediated gene repression has revealed new perspectives into the pathogenesis of testosterone insufficiency, including mitochondrial dysfunction, inflammation, steroidogenic impairment, cellular proliferation, and apoptosis. This review aims to understand the underlying mechanisms and interrelations between miRNAs and Leydig cell physiology/pathophysiology, which will enlighten innovative and effective strategies for hypogonadism-associated male infertility.
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Jothiraman et al. (2026) studied this question.
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