The male reproductive system’s development and function are intricately linked to complex hormonal interactions, with the HPG axis’s pulsatile hormone release playing a key role in male fertility. These cells are essential for spermatogenesis and necessitate a precise combination of hormones, growth factors, and other signals for successful development . Additionally, hormones play a crucial role in sexual function and spermatogenesis, and while there has been extensive research on the targets and functions of hormonal regulation, the endeavor to simulate these processes in vitro presents significant challenges.
Such holistic perspectives are imperative not just for solving reproductive health issues but also for advancing our understanding of systemic endocrine functions. In addition, dysfunction in hormonal signaling is not without repercussions. Cartoon depicting an adult mouse testis, showing localization of hormone receptors in different cell types and known (solid lines) and putative (dashed lines) interactions between cell types. The impact of nuclear receptor signaling pathways, such as those mediated by steroid hormone receptors, is profound.
Progesterone rapidly activates intracellular signaling in human sperm, regulating key aspects of their physiology (Publicover and Barratt, 2011). Analysis of human testicular morphology and function after estradiol treatment revealed decreased seminiferous tubule diameter and induced fatty degeneration in the surrounding connective tissue. Following chronic treatment with estradiol, however, a reduced number of germ cells was observed, likely caused by increased germ cell apoptosis (Kaushik et al., 2010b).
This intricate barrier segregates the seminiferous tubules from the bloodstream, effectively restricting the diffusion of water, ions, electrolytes, paracrine factors, hormones, and other exogenous biomolecules through both the paracellular and transcellular pathways. These peptides facilitate communication between Sertoli cells and germ cells to support spermatogenesis and fertility 4,5. Seminiferous tubules are home to germ cells, which are crucial for spermatogenesis, as well as Sertoli cells and peritubular myoid cells (PMCs). The junctions between Sertoli cells form the BTB, which provides an immunologically privileged environment for spermatogenesis. In the process of spermatogenesis, germ cells (spermatogonia, pre-leptotene spermatocytes, pachytene spermatocytes, round spermatid, and elongating spermatid) move in the seminiferous epithelium and undergo meiosis until they are released to the seminiferous tubular fluid.
In contrast, ERβ expression in mouse testes reaches its zenith on postnatal days 1–5 and is seldom seen after postnatal day 12 (Cooke et al., 2017). However, the expression dynamics of ERα in mouse testes show a decline from mid to late puberty (Jefferson et al., 2000). The classical pathway involves the nuclear estrogen receptors ERα (ESR1) or ERβ (ESR2) (King and Greene, 1984; Green et al., 1986; Greene et al., 1986; Kuiper et al., 1996). Letrozole, an aromatase inhibitor, causes estrogen deficiency and androgen excess.
In immature male rats, the prolonged suppression of PRL can inhibit the process of spermatocyte–spermatid conversion, alter Leydig cell morphology, and increase serum LH levels. Despite the recognized detrimental impact of estrogen on male fertility over the years, the appropriate expression of estrogen still plays a significant role in male reproductive capability and should not be overlooked. However, adult male rats exposed to a diet high in phytoestrogens also experienced increased germ cell apoptosis and disruptions in spermatogenesis . Additionally, INSL3 has been found to inhibit germ cell apoptosis by binding to leucine-rich repeat-containing G protein-coupled receptor 8 (LGR8), which is expressed in germ cells 130,131,132. The expression of INSL3 is directly dependent on the number and differentiation status of Leydig cells and is an ideal biomarker for Leydig cells . INSL3 belongs to the insulin–relaxin family and is primarily produced in Leydig cells in human males . As puberty progresses, Sertoli cells transition from a proliferative, immature state to a mature, quiescent one, leading to a marked decrease in AMH levels .
PMCs play a role in regulating sperm and luminal fluid transport and secrete growth factors and an extracellular matrix to uphold the niche of spermatogonial stem cells (SSCs). The microenvironment created by neighboring Sertoli cells is vital for maintaining germ cell growth and initiating differentiation 3,4. The most optimal energy source for developing germ cells, the lactate molecule, is provided by Sertoli cells, which also furnish necessary growth factors and chemokines.

性別: 女

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