Follicle-Stimulating Hormone Exacerbates Cardiovascular Disease in the Presence of Low or Castrate Testosterone Levels

Wilhelmina C.M. Duivenvoorden, David Margel, Vishal Subramony Gayathri, Emmanuelle Duceppe, Sadiya Yousef, Magda Naeim, Mohammad Khajehei, Sarah Hopmans, Snezana Popovic, Yaara Ber, Diane Heels-Ansdell, Philip J. Devereaux, Jehonathan H. Pinthus*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

1 Scopus citations


Low testosterone (T), common in aging men, associates with cardiovascular disease. We investigated whether follicle-stimulating hormone (FSH), which is affected by T, modulates the cardiovascular effects associated with low T or castration. FSHβ−/−:low-density lipoprotein receptor (LDLR)−/− mice, untreated or castrated (orchiectomy, gonadotropin-releasing hormone agonist or antagonist), demonstrated significantly less atherogenesis compared with similarly treated LDLR−/− mice, but not following FSH delivery. Smaller plaque burden in LDLR−/− mice receiving gonadotropin-releasing hormone antagonists vs agonists were nullified in FSHβ−/−:LDLR−/− mice. Atherosclerotic and necrotic plaque size and macrophage infiltration correlated with serum FSH/T. In patients with prostate cancer, FSH/T following androgen-deprivation therapy initiation predicted cardiovascular events. FSH facilitates cardiovascular disease when T is low or eliminated.

Original languageEnglish
Pages (from-to)364-379
Number of pages16
JournalJACC: Basic to Translational Science
Issue number3
StatePublished - Mar 2024


  • GnRH-antagonist
  • androgen-deprivation therapy
  • cardiovascular disease
  • follicle-stimulating hormone
  • prostate cancer


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