Miguel A. Aon

TL;DR: The transitions in mitochondrial energetics were tightly coupled to activation of sarcolemmal KATP currents, causing oscillations in action potential duration, and thus might contribute to catastrophic arrhythmias during ischemia-reperfusion injury.

TL;DR: The model closely reproduces experimentally observed mitochondrial NADH dynamics in heart trabeculae subjected to changes in pacing frequency and supports the hypothesis that mitochondrial matrix Ca(2+) plays an important role in matching energy supply with demand in cardiac myocytes.

TL;DR: The authors' data illustrate the complexity of CR in the context of aging, with a clear separation of outcomes related to health and survival, highlighting complexities of translation of CR into human interventions.

TL;DR: The results indicate that mitochondria take up Ca2+ rapidly and contribute to fast buffering during a [Ca2+]c transient; and elevated Na+ ([Na+]i) impairs mitochondrial Ca2- uptake, with consequent effects on energy supply and demand matching.

TL;DR: It is postulated that mitochondria have been evolutionarily optimized to maximize energy output while keeping ROS overflow to a minimum by operating in an intermediate redox state, and the continuum described by the model has the potential to account for many disparate experimental observations and also provides a rationale for graded physiological ROS signaling at redox potentials near the minimum.