Raw data for the article entitled "Derivatization-Enhanced Thiol Redox Atlas Reveals ENO1-SLC7A11 Axis as Ferroptosis Protector in Myocardial Injury"

Myocardial injury creates intense redox stress accompanied by thiol metabolites as molecular redox buffers. Given their limited analytical sensitivity, global detection and functional characterization of thiol networks remain a major bottleneck. Here we develop a derivatization-enhanced mass spectrometry imaging method, assisted by a Python-based annotation platform, to construct a cross-species thiol redox atlas with spatial resolution. We identified 405 thiols, including 170 species not previously documented in public metabolomic databases, and first show that endogenous thiol pool is highly tissue- and region-specific. In the isoproterenol-induced rat model of myocardial injury, heart damage causes distinctive thiol metabolism patterns, especially previously overlooked noncanonical cysteine-derived, long-chain, and substituted thiols. Similar thiol shifts are observed in serum from patients with myocardial infarction. Upon myocardial injury, multi-omics integration highlights enolase 1 (ENO1) as a thiol-linked hub in cardiomyocytes. ENO1 inhibition weakens SLC7A11 induction, depletes glutathione, and aggravates iron-dependent lipid damage. Biochemical assays support a stress-inducible ENO1-SLC7A11 interaction that promotes cystine-driven thiol replenishment, suggesting promising targets for cardioprotective therapy.