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Leydig cell insufficiency in hypospermatogenesis: a paracrine effect of activin–inhibin signaling?
Author(s) -
Winters S. J.,
Moore J. P.,
Clark B. J.
Publication year - 2018
Publication title -
andrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.947
H-Index - 43
eISSN - 2047-2927
pISSN - 2047-2919
DOI - 10.1111/andr.12459
Subject(s) - paracrine signalling , sertoli cell , leydig cell , endocrinology , medicine , testosterone (patch) , biology , autocrine signalling , spermatogenesis , microbiology and biotechnology , hormone , receptor , luteinizing hormone
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.