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1 Introduction Cardiometabolic syndrome (CMS) is defined by the clustering of central obesity, insulin resistance, atherogenic dyslipidemia, hypertension, and chronic low-grade inflammation, a constellation that markedly increases the risk of type 2 diabetes, cardiovascular disease, and premature mortality (1)

Furthermore, mechanistic studies investigating the GSH-susceptibility of succinimide thioether bonds found the type of thiol and N -substituent used to play key roles in the rate of cleavage of succinimide thioether linkages in reducing environments, where N -substituents capable of forming more hydrogen bonds and thiol groups of low pKas led to greater rates of bond cleavage in GSH [48]

The analysis of the subphenotype revealed that the treatment decreased the number of M2 macrophages that were identified as the profibrotic phenotype (Fig

Consistently, single-cell RNA sequencing (scRNA-seq) analysis showed that FSP1 is predominantly expressed in monocytes/macrophages (Fig