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Mechanistic studies of redox dysfunction remain challenging due to limited strategies that can perturb redox metabolism in various cellular or organismal backgrounds. Most studies involving impaired redox metabolism have focused on oxidative stress; consequently, less is known about the settings where there is an overabundance of NADH reducing equivalents also known as reductive stress. In an article in Nature Chemical Biology @nchembio today, we are introducing a new genetically encoded tool to increase cellular NADH/NAD+ ratio which we named EcSTH. Using EcSTH, we determined that metabolic and transcriptomic signatures of the NADH reductive stress (aka high NADH/NAD+ ratio) are cellular background specific. For example, we show that, under the NADH reductive stress, non-oxidative PPP, purine biosynthesis and GDF15 metabokine levels are upregulated. Another interesting implication of our work is that reductive stress can also result in the accumulation of noncanonical sugar phosphates, which are known to be toxic. We anticipate that EcSTH tool will be useful for investigating redox metabolism in various cellular and organismal contexts and disease states, including aging-associated metabolic changes! @XingxiuPan @MinaLorrain @saraviolante @russpgoodman Check out the full version of the paper below for details: rdcu.be/dpypb or nature.com/articles/s41589-0… Supported by: @Scintillon @scrippsresearch @NIGMS @NIDDKgov