Unrestrained fatty acid oxidation triggers heart failure in mice via cardiolipin loss and mitochondrial dysfunction.

However, succinate-driven H 2 O 2 release (reflecting reverse electron transport at complex I) was reduced relative to WT, TBARS levels were unchanged, and the trend toward increased protein carbonylation did not reach statistical significance ( Supplemental Figure 2 , H–K).

also in 111,027 other papers