Elucidating the role of sodium-myo-inositol co-transporter-1 (SMIT1) in cardiac dysfunction

Sodium-myo-inositol cotransporter-1, SMIT1, promotes cardiac hypertrophy and fibrosis induced by pressure overload in mice

Cardiovascular Research

In patients with heart failure, plasma levels of myo-inositol are elevated.

In this study, Marino et al. revealed that the sodium-myo-inositol cotransporter 1 (SMIT1), a member of the sodium/glucose co-transporters (SGLT) family, facilitates myo-inositol uptake into cardiac myocytes, promoting Na+ accumulation and inositol 1,4,5-trisphosphate (IP3)- and Ca2+-dependent pro-hypertrophic signalling.

Deletion of SMIT1 protects from heart failure through upregulation of carabin, which inhibits calcineurin/NFAT and Ras/ERK1/2 signaling to prevent maladaptive remodeling. Read the full study to discover why SMIT1 may be a novel therapeutic target to treat heart failure.