To live or to die is one of the most delicate decisions on a cellular level. Environmental signals are constantly integrated and can activate a multitude of pathways that either activate life-saving countermeasures or initiate cell death programs. On an organismal level, both life-saving and life-terminating mechanisms on cellular level are of central importance and play essential roles during diverse processes including growth, tissue regeneration or immune responses.

Prominent signaling messengers with multiple intracellular functions are reactive oxygen species (ROS). ROS lead to proliferation and survival of cells. However, unbalanced protein folding, energy production or fatty acid metabolism resulting from tumorigenic processes, viral infections or inflammation, trigger a pathological increase of ROS levels leading to oxidative stress [1]. While multiple enzymatic and non-enzymatic mechanisms have evolved to protect cells from such detrimental accumulation of ROS, the molecular mechanisms by which ROS sensing translates into anti-inflammatory or cytotoxic programs remain incompletely understood. It was shown that ROS can cause activation of necroptosis, the inflammasome pathway and caspase-dependent cell death, but a molecular sensor for intracellular ROS was not known. Recently, we identified “oxeiptosis”, a signaling pathway that couples a ROS sensor to a non-canonical cell-death execution pathway [2].

Log in or create a free account to read this content

Gain free access to this article, as well as selected content from this journal and more on nature.com

Access through your institution

or

Sign in or create an account
Continue with Google
Continue with ORCiD