Drug development hypertrophy

NF-AT3 also cooperates with GATA-4, a heart-specific transcription factor. When Ca2+ levels rise in a stressed heart, NF-AT3 moves to the nucleus and binds to GATA-4 and both turn on genes responsible for cardiac hypertrophy. The clinical importance of cardiac hypertrophy, which eventually causes heart failure, makes the development of drugs that act like immunosuppressives, preventing nuclear import of NF-AT3, an active area of research into control of cardiac hypertrophy. ... 

Other 0,-AR subtypes have also been proposed. In particular, Muramatsu et al. [12] described an a AR subtype exhibiting a low affinity for prazosin. This subtype has recently been proposed to mediate the contraction of prostatic smooth muscle [18] and therefore could play a key role in the development of more effective drug therapies to treat benign prostatic hypertrophy. Unfortunately, it has been difficult to identify this subtype with radioligand binding approaches, and its relationship to the cloned subtypes is currently unknown. More selective compounds, further functional studies, and the cloning of this receptor subtype will help to clarify this issue. 

An AIDS patient who is being treated with multiple drugs, including AZT, lamivudine, indinavir, ketoconazole, and TMP-SMX, develops breast hypertrophy, central adiposity, hyperlipidemia, insulin resistance, and nephrolithiasis. If these changes are related to his drug treatment, the most likely cause is... 

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