Redox Sensing and Cardiac Myocyte Loss: Some Recent Insights

Abstract

Generation of reactive oxygen-nitrogen species (ROS/RNS) has long been ascribed to pathophysiological conditions like ageing, neurodegenerative and cardiovascular disorders. However, more recent evidences suggest that while generation of ROS/RNS at a higher threshold is deleterious, at a lower dose these can act as second messengers, influencing specific cellular events like cell growth and differentiation, embryonic development, protection against ischemic injuries and progression of diseases like cancer. With the advent of sophisticated tools of biochemistry and cell biology, it is becoming apparent that various ROS/RNS, when generated transiently at a moderate level, can reversibly modify proteins, causing loss-gain of functions, analogous to that by phosphorylation-dephosphorylation. More significantly, recent studies also suggest that even apoptosis induced by ROS/RNS might also involve discrete cell signaling rather than general surge of ROS/RNS as the dterminant. Taken together, coming days are likely to reveal more discrete nature of ROS/RNS signaling in various cellular contexts including cell death.