Scientists show that when a molecule known as c-Jun N-terminal kinase (JNK) becomes active in sepsis, it increases the production of a protein called B-type natriuretic peptide (BNP) — the more BNP that is produced in sepsis, the greater the deterioration of cardiovascular function. But perhaps more significantly, in mice, the researchers show that JNK and BNP activity can be halted, reversing cardiovascular damage and reducing the risk of death from sepsis.
