Succinate metabolism: a new therapeutic target for myocardial reperfusion injury.
Level 5 - mechanism / opinion, no new human data
Narrative review of mechanistic and preclinical metabolic pathways with no clinical data.
PubMed 27194563 · doi:10.1093/cvr/cvw100
What was done
This review examined the literature on metabolic mechanisms in myocardial ischemia/reperfusion injury, focusing on how the citric acid cycle intermediate succinate accumulates during ischemia, drives mitochondrial reactive oxygen species production via reverse electron transport at Complex I upon reperfusion, and can be targeted therapeutically.
What was found
The abstract reports no numerical data or quantitative effect estimates. It presents a mechanistic model where succinate accumulation during ischemia underlies elevated reactive oxygen species at reperfusion and suggests that targeting this metabolic pathway may confer cardioprotection.
Why it matters
Myocardial ischemia/reperfusion injury lacks effective clinical therapies. Identifying succinate metabolism as a central driver of reperfusion damage outlines a specific metabolic target for drug development.
Limits
This is a narrative review with no primary empirical data or human clinical trial results presented in the abstract. The underlying findings derive primarily from bench and animal models, and clinical efficacy in patients remains to be tested.
Cited by
- supports When a person suffers a heart attack and stops breathing, the bloodstream fills with lactic acid and succinic acid.