Mitochondrial energetics and calcium coupling in the heart.
Level 5 - mechanism / opinion, no new human data
Narrative review describing mechanistic concepts without original experimental or clinical data
PubMed 28105746 · doi:10.1113/JP273609
What was done
This narrative review summarizes mechanistic concepts regarding cardiac mitochondrial bioenergetics, focusing on how ADP and calcium signals coordinate oxidative phosphorylation to match myocardial energy supply with demand, and how dysregulation contributes to heart failure pathophysiology.
What was found
No quantitative data or numerical findings are reported in the abstract. Mechanistically, heart failure involves an imbalance between ADP and calcium that causes oxidation of mitochondrial pyridine nucleotides; NADH oxidation limits ATP synthesis and contractile function, while NADPH oxidation promotes oxidative stress and maladaptive cardiac remodeling.
Why it matters
Understanding the failure of mitochondrial calcium-energetics coupling highlights potential metabolic and redox targets for heart failure therapy beyond classical neuroendocrine inhibition.
Limits
As a narrative review, the paper provides theoretical and mechanistic synthesis rather than original clinical or empirical data. The abstract reports no sample size, controlled experimental cohorts, or quantitative outcome measures.
Cited by
- supports Both myocardial contraction (systole) and myocardial relaxation (diastole) require active energy consumption.