Hearts have a hidden mitochondrial lactate route that backs up pyruvate import
- Mouse hearts still oxidize glucose carbon without the pyruvate carrier, via a parallel lactate route through MCT1.
- MCT1 sits in the inner mitochondrial membrane of mouse and human cardiomyocytes, pairing with matrix LDHB to convert lactate to pyruvate and NADH for respiration.
- Removing MCT1 impairs metabolic flexibility and worsens heart failure and survival under neurohormonal or ischemia-reperfusion stress.
💡 Points Based on the abstract
Treat this as a cardiac safety flag, not a target. The phenotype only surfaces under stress, so a clean baseline echo would miss it, and MCT1 inhibitors already in oncology block plasma-membrane and mitochondrial lactate flux alike. I'd want adult, cardiomyocyte-restricted deletion, human loss-of-function data and cardiac exposure margins before trusting any of it.
MCT1-dependent mitochondrial lactate import sustains cardiac metabolism ↗