bims-resufa Biomed news
on Respiratory Supercomplex Factors
Issue of 2018‒04‒15
one paper selected by
Josh Garlich
Medical College of Wisconsin

  1. J Mol Biol. 2018 Apr 04. pii: S0022-2836(18)30176-1. [Epub ahead of print]
    Berry BJ, Trewin AJ, Amitrano AM, Kim M, Wojtovich AP.
      Mitochondrial respiration results in an electrochemical proton gradient, or protonmotive force (pmf), across the mitochondrial inner membrane (IM). The pmf is a form of potential energy consisting of charge (∆ψm) and chemical (∆pH) components, that together drive ATP production. In a process called uncoupling, proton leak into the mitochondrial matrix independent of ATP production dissipates the pmf and energy is lost as heat. Other events can directly dissipate the pmf independent of ATP production as well, such as chemical exposure or mechanisms involving regulated mitochondrial membrane electrolyte transport. Uncoupling has defined roles in metabolic plasticity and can be linked through signal transduction to physiologic events. In the latter case, the pmf impacts mitochondrial reactive oxygen species (ROS) production. Though capable of molecular damage, ROS also have signaling properties that depend on the timing, location, and quantity of their production. In this review we provide a general overview of mitochondrial ROS production, mechanisms of uncoupling, and how these work in tandem to affect physiology and pathologies, including: obesity, cardiovascular disease, and immunity. Overall, we highlight that isolated bioenergetic models-mitochondria and cells-only partially recapitulate the complex link between the pmf and ROS signaling that occurs in vivo.
    Keywords:  T cells; brown adipose tissue; ischemia reperfusion injury; mitochondria; proton leak