The mitochondrion is a complex organelle essential for
energy transduction, ATP production, and multiple cellular signaling events.
A finely tuned regulatory network controls the biogenesis, maintenance, and turnover of mitochondria.
In the heart, this high-capacity mitochondrial system dynamically generates and consumes enormous amounts of ATP
to support continuous pumping in response to changing energy demands1.
To sustain constant ATP production, malfunctioning mitochondria are continuously replaced by newly synthesized organelles
through processes involving mitochondrial biogenesis, replication, and autophagy/mitophagy2,3.
These processes are tightly regulated, with mitochondrial fusion and fission allowing the formation and remodeling
of a reticulated mitochondrial network4.
Since mitochondria are responsible for ATP generation, any agent interfering with physiological mitochondrial function in the myocardium
may deplete the cellular ATP pool, potentially leading to myocardial dysfunction.
Quantitative assessment of mitochondrial health is critical to evaluate potential cardioprotective compounds and detect unwanted cardiotoxic effects.