Extracellular vesicles from hypoxia-preconditioned mesenchymal stem cells alleviates myocardial injury by targeting thioredoxin-interacting protein-mediated hypoxia-inducible factor-1α pathway

Figure 9 During myocardial infarction or hypoxia, hypoxia-inducible factor-1 alpha export is chromosomal region maintenance-1-dependent in the presence of thioredoxin-interacting protein, based on the association of thioredoxin-interacting protein with chromosomal region maintenance-1. Thioredoxin-interacting protein (TXNIP)-induced hypoxia-inducible factor-1 alpha (HIF-1α) nuclear export may be hypoxia-independent, which triggers ubiquitination and degradation by the proteasome in cardiomyocytes. As a transcription factor, the function of HIF-1 in promoting targeted gene transcription is abolished by hypoxia/myocardial infarction-triggered TXNIP activation. Our research aimed to clarify this process by hypoxia-preconditioned extracellular vesicles and the underlying mechanism.