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Nov 8 2003;362(9395):1527-35
In adults, mature erythrocytes develop as a result of erythropoiesis from bone marrow-located hematopoietic stem cells through a gradual and consequent process that includes stepwise formation of myeloid progenitors, megakaryocytic-erythroid progenitors, burst-forming unit-erythroids (BFU-e) and colony-forming unit-erythroids (CFU-e), proerythroblasts, basophilic, polychromatic, and orthochromatic erythroblasts, reticulocytes, and eventually mature erythrocytes [30, 31]
But if androgen receptor density is such a dominant driver of anabolic response, how do you reconcile this with the fact that chronic low-grade inflammation (particularly via IL-6/STAT3 and TNF-/NF-B signaling) can suppress AR nuclear translocation even when receptor count is high and that in some individuals this blunts hypertrophy more dramatically than CAG-repeat length or hormone levels themselves?
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