Tissue receptivity refers to the functional sensitivity of target cells and organs to circulating hormones, representing the final, crucial step in the endocrine signaling cascade. This sensitivity is determined by the concentration, affinity, and proper function of specific hormone receptors on or within the target cell. Optimal tissue receptivity is essential for a hormone to exert its intended biological effect, irrespective of adequate hormone levels in the blood.
Origin
This term is rooted in cell biology and receptor pharmacology, where the concept of a hormone-receptor interaction dictates the magnitude of the biological response. ‘Receptivity’ emphasizes the target tissue’s active role in responding to the hormonal signal, moving beyond a simple focus on circulating hormone concentrations. Clinical conditions like insulin resistance are prime examples of impaired tissue receptivity.
Mechanism
Receptivity is mechanistically regulated by several factors, including receptor density, which can be upregulated or downregulated in response to chronic hormone exposure, and receptor phosphorylation status. Furthermore, coactivator and corepressor proteins modulate the nuclear receptor’s ability to initiate gene transcription upon hormone binding. Impaired receptivity, such as the downregulation of androgen receptors due to chronic stress, can lead to symptoms of hormone deficiency even when blood levels appear normal.
Senolytics can enhance hormonal optimization by clearing senescent cells, reducing inflammation, and improving tissue receptivity to endocrine signals.
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