Testicular Pathology and Hormonal Function

Testicular pathology encompasses a spectrum of structural and cellular disorders that compromise the gonad’s ability to support spermatogenesis and endocrine activity. Central to testicular function are the somatic Leydig and Sertoli cells: Leydig cells synthesise and secrete androgens under luteinising hormone control, while Sertoli cells nurture germ cells and produce paracrine factors that regulate tubular microenvironments. Disruption of this finely balanced system—whether through inflammation, fibrosis, neoplasia or environmental insults—can manifest as impaired sperm production, hormonal imbalance and infertility. Hormonal function relies on feedback loops involving the hypothalamus and pituitary, with key markers such as anti-Müllerian hormone and inhibin B reflecting Sertoli cell health and spermatogenic status. Emerging evidence highlights the role of immune-mediated orchitis, interstitial remodelling and endocrine disruptors in driving pathophysiology. Advances in molecular profiling and imaging have elucidated mechanisms of germ cell loss, Leydig cell dysfunction and paracrine dysregulation, reinforcing the need for integrated diagnostic and therapeutic approaches. The global decline in male reproductive health underscores the urgency of bridging basic pathology with clinical endocrinology to preserve fertility and hormonal well-being.

Research from Nature Portfolio

Recent studies in canine models have illuminated the relationship between circulating and seminal biomarkers of testicular cell function and semen quality. Quantitative assessment of anti-Müllerian hormone, inhibin B, testosterone, free androgen index and insulin-like peptide 3 revealed distinct correlations with sperm count, motility and morphology. Age and testicular consistency emerged as predictors of declining semen parameters, while elevated alkaline phosphatase activity aligned with higher sperm output. Notably, systemic anti-Müllerian hormone levels were linked to adverse head defects, and serum testosterone inversely correlated with age. These findings refine our understanding of Sertoli and Leydig cell contributions to spermatogenic competence and suggest that combined hormonal profiling may enhance the diagnostic evaluation of male infertility.

Testicular Pathology and Hormonal Function publication trend

The graph below shows the total number of articles in testicular pathology and hormonal function across all publications each year (not limited to Nature Index journals).

Technical terms

Leydig cells: Interstitial testicular cells responsible for androgen synthesis in response to luteinising hormone.

Sertoli cells: Somatic cells within seminiferous tubules that support germ cell maturation and secrete growth factors.

Spermatogenesis: The multi-stage process by which germ cells differentiate into mature spermatozoa.

Azoospermia: The absence of spermatozoa in ejaculate, classified as obstructive or non-obstructive.

Orchitis: Inflammation of the testis, which may be immune-mediated or infectious in origin.

Anti-Müllerian hormone: Glycoprotein produced by Sertoli cells that reflects immature Sertoli cell activity and spermatogenic potential.

Inhibin B: Peptide hormone secreted by Sertoli cells that provides negative feedback on follicle-stimulating hormone secretion.

References

1. Endocrine and dog factors associated with semen quality. Scientific Reports (2024).
2. Comprehensive Analysis of the Association Between Human Non-obstructive Azoospermia and Plasticisers via Single-Cell and Traditional RNA Sequencing Methods. Exposure and Health (2022).
3. Leydig Cells in Patients with Non-Obstructive Azoospermia: Do They Really Proliferate?. Life (2021).
4. The Fate of Leydig Cells in Men with Spermatogenic Failure. Life (2022).