Leydig cell aging: Molecular mechanisms and treatments

V. Papadopoulos, B. R. Zirkin

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Late-onset hypogonadism, resulting from deficiency in serum testosterone (T), affects the health and quality of life of millions of aging men. T is synthesized by Leydig cells (LCs) in response to luteinizing hormone (LH). LH binds LC plasma membrane receptors, inducing the formation of a supramolecular complex of cytosolic and mitochondrial proteins, the Steroidogenic InteracTomE (SITE). SITE proteins are involved in targeting cholesterol to CYP11A1 in the mitochondria, the first enzyme of the steroidogenic cascade. Cholesterol translocation is the rate-determining step in T formation. With aging, LC defects occur that include changes in SITE, an increasingly oxidative intracellular environment, and reduced androgen formation and serum T levels. T replacement therapy (TRT) will restore T levels, but reported side effects make it desirable to develop additional strategies for increasing T. One approach is to target LC protein-protein interactions and thus increase T production by the hypofunctional Leydig cells themselves.

Original languageEnglish (US)
Title of host publicationVitamins and Hormones
PublisherAcademic Press Inc.
DOIs
StateAccepted/In press - 2021

Publication series

NameVitamins and Hormones
ISSN (Print)0083-6729

Keywords

  • Androgen
  • Hormone action
  • Late-onset hypogonadism
  • Mitochondria
  • Oxidant/antioxidant balance
  • Protein-protein interactions
  • Steroid hormones
  • Testosterone

ASJC Scopus subject areas

  • Physiology
  • Endocrinology

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