Molecular ‘palpation’ of BPH: a tale of MAPK signalling?

Benign prostatic hyperplasia (BPH) is a very common cause of hospitalization and surgery is currently the most effective therapy. MAP kinases (MAPKs) are a group of protein kinases with an important function in integrating physiological and pathological stimuli that might impact on cellular growth, differentiation and programmed cell death (apoptosis). Certain components of the MAPK signal-transduction pathways are involved in stimulus-specific fine-tuning of the activities mediated by the various MAPK families. As homeostasis is impaired in the hyperplastic prostate, aberrant coordination of the MAPK cascades might be implicated in a proliferative–apoptotic imbalance. Here, we hypothesize that the pathogenesis of BPH might be facilitated by functional anomalies in the MAPK circuitry and postulate that pharmacological ‘rewiring’ of MAPK pathways offers a potentially exciting new avenue for improved therapeutic control of clinical BPH.