Leydig cell insufficiency in hypospermatogenesis: a paracrine effect of activin–inhibin signaling?

Leydig cell insufficiency in hypospermatogenesis: a paracrine effect of activin–inhibin signaling?

Summary Clinical findings and a variety of experimental models indicate that Leydig cell dysfunction accompanies damage to the seminiferous tubules with increasing severity. Most studies support the idea that intratesticular signaling from the seminiferous tubules to Leydig cells regulates steroidog...

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Veröffentlicht in:Andrology (Oxford) 2018-03, Vol.6 (2), p.262-271
Hauptverfasser: Winters, S. J., Moore, J. P., Clark, B. J.
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Sprache:eng
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activin
hypospermatogenesis
inhibin
Leydig cell
testosterone
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Moore, J. P.
Clark, B. J.
description Summary Clinical findings and a variety of experimental models indicate that Leydig cell dysfunction accompanies damage to the seminiferous tubules with increasing severity. Most studies support the idea that intratesticular signaling from the seminiferous tubules to Leydig cells regulates steroidogenesis, which is disrupted when hypospermatogenesis occurs. Sertoli cells seem to play a pivotal role in this process. In this review, we summarize relevant clinical and experimental observations and present evidence to support the hypothesis that testicular activin signaling and its regulation by testicular inhibin may link seminiferous tubular dysfunction to reduced testosterone biosynthesis.
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subjects activin
hypospermatogenesis
inhibin
Leydig cell
testosterone
title Leydig cell insufficiency in hypospermatogenesis: a paracrine effect of activin–inhibin signaling?
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