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Mitochondrial energetics and calcium coupling in the heart
Author(s) -
Kohlhaas Michael,
Nickel Alexander G.,
Maack Christoph
Publication year - 2017
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jp273609
Subject(s) - oxidative phosphorylation , mitochondrion , oxidative stress , calcium , heart failure , biophysics , chemistry , contraction (grammar) , respiration , adenosine triphosphate , biochemistry , medicine , microbiology and biotechnology , endocrinology , biology , anatomy
Contraction and relaxation of the heart consume large amounts of energy that need to be replenished by oxidative phosphorylation in mitochondria, and matching energy supply to demand involves the complimentary control of respiration through ADP and Ca 2+ . In heart failure, an imbalance between ADP and Ca 2+ leads to oxidation of mitochondrial pyridine nucleotides, where NADH oxidation may limit ATP production and contractile function, while NADPH oxidation can induce oxidative stress with consecutive maladaptive remodelling. Understanding the complex mechanisms that disturb this finely tuned equilibrium may aid the development of drugs that could ameliorate the progression of heart failure beyond the classical neuroendocrine inhibition.