Title : Testosterone Deficiency Promotes Hypercholesteremia and Attenuates Cholesterol Liver Uptake via AR/PCSK9/LDLR Pathways.

Pub. Date : 2022

PMID : 35599686






5 Functional Relationships(s)
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1 Further investigation revealed that lack of testosterone induced increased proprotein convertase subtilisin/kexin type 9 (PCSK9) and decreased low-density lipoprotein receptor (LDLR) both in vivo and in vitro. Testosterone proprotein convertase subtilisin/kexin type 9 Homo sapiens
2 Further investigation revealed that lack of testosterone induced increased proprotein convertase subtilisin/kexin type 9 (PCSK9) and decreased low-density lipoprotein receptor (LDLR) both in vivo and in vitro. Testosterone proprotein convertase subtilisin/kexin type 9 Homo sapiens
3 Moreover, the androgen receptor (AR) antagonist flutamide mimicked the effects of testosterone deficiency on PCSK9 and LDLR indicating the role of AR as a mediator in triggering attenuating liver cholesterol uptake in which testosterone instead of dihydrotestosterone (DHT) is the major functional form of androgen. Testosterone proprotein convertase subtilisin/kexin type 9 Homo sapiens
4 Conclusion: Testosterone deficiency attenuated cholesterol liver uptake mediated by the PCSK9-LDLR pathway, in which AR and testosterone without transforming to DHT play important roles. Testosterone proprotein convertase subtilisin/kexin type 9 Homo sapiens
5 Conclusion: Testosterone deficiency attenuated cholesterol liver uptake mediated by the PCSK9-LDLR pathway, in which AR and testosterone without transforming to DHT play important roles. Testosterone proprotein convertase subtilisin/kexin type 9 Homo sapiens