Txnip C247S Mutation Improves Cardiac Function in Diabetes

<p class="MsoNoSpacing" style="margin:0in 0in 0pt;"> This is a story about a good guy (thioredoxin) vs. a bad guy (Txnip). Consulting Editor Paras Mishra (University of Nebraska Medical Center) interviews lead author Jun Yoshioka (City University of New York) and expert Rebecca Ritchie (Monash University) about the latest research by Yoshioka and co-authors. As the underlying basis of diabetic cardiomyopathy remains unclear, Mukai et al. focused on the pathway connecting hyperglycemia to oxidative stress. Thioredoxin is an antioxidant molecule which uses catalytic sites at cysteine 32 and 35 to reduce target proteins and detoxify oxidative stress. The villain Txnip, an endogenous inhibitor of thioredoxin and its antioxidative properties, acts as a pro-oxidant. A high level of extracellular glucose strongly upregulates Txnip. “If glucose induces Txnip, and Txnip is a bad guy killing cells, then the obvious question is: does Txnip mediate diabetes-induced cellular damage?” explains Yoshioka. What’s the answer? Listen now.</p> <p class="MsoNoSpacing" style="margin:0in 0in 0pt;"> </p> <p class="MsoNoSpacing" style="margin:0in 0in 0pt;"> Nobuhiro Mukai, Yoshinobu Nakayama, Syed Amir Abdali, Jun Yoshioka <a href='https://doi.org/10.1152/ajpheart.00174.2021'> Cardiomyocyte-specific Txnip C247S mutation improves left ventricular functional reserve in streptozotocin-induced diabetic mice </a> Am J Physiol Heart Circ Physiol, published June 4, 2021. DOI: 10.1152/ajpheart.00174.2021</p>