The fundamental process by which lipid-soluble steroid hormones, such as cortisol, testosterone, and estrogen, traverse the cell membrane and bind to specific intracellular receptors, forming a hormone-receptor complex that then translocates to the nucleus to directly modulate gene transcription. This genomic signaling pathway is slow but powerful, governing long-term changes in cellular differentiation, metabolism, and physiological function. It is the core mechanism of action for all steroid-derived hormones.
Origin
This is a cornerstone concept in classical endocrinology, combining the chemical class “Steroid Hormone” with the cellular communication process “Signaling.” It describes the unique lipophilic nature of these hormones and their direct interaction with the cell’s genetic machinery.
Mechanism
The signaling cascade begins with the hormone passively diffusing across the plasma membrane due to its lipophilicity. Once inside, it binds to its high-affinity receptor, releasing heat shock proteins and inducing a conformational change. This activated complex then binds to specific DNA sequences, known as Hormone Response Elements, located near target genes. This binding event either enhances or suppresses the transcription of those genes, ultimately altering the cellular proteome and producing the long-lasting physiological effect of the hormone.
Compounded hormones remain essential by offering the pharmacokinetic precision required to tune the body's complex endocrine and metabolic signaling pathways.
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