RESUMO
Since its discovery in the 1970s, the mitochondrial permeability transition(mPT)has been proposed to be a strategic regulator of programmed cell death(PCD). The mPT denotes an increase in the mitochondrial inner membrane permeability to solutes with molecular masses up to about 1.5×103. It is presumed to be mediated by an opening of a channel, the mPT pore(mPTP), whose molecular nature remains a mystery. Intense research efforts have focused on elucidating the molecular components of the mPTP because it may help to better understand and treat various pathologies ranging from neurodegenerative and cardiac diseases to cancer. This article briefly reviews the new progress of mPTP structural models and its specific molecular mechanisms of regulating PCD, then demonstrates the feasibility of using the mPTP-targeting agents as a potential alternative strategy for effective management of PCD.