Table 1.

Key features of cardiac hypertrophy and the mitochondrial alterations.

	Cardiac homeostasis	Cardiac hypertrophy
Stimuli	None	Cardiac volume/pressure overload, Ang II, oxidants, activation of α/β adrenergic receptors, hypoxia, aging, high-glucose, and etc.
Cardiac structure	Normal	Enlarged cardiomyocytes, increased heart wall thickness and heart mass, interstitial fibrosis, and increased cellular apoptosis
Cardiac function	Normal	Impaired
Mitochondrial structure	Rich and intact, with complete membrane structures and clear cristae structures	Swollen and deformed, with blurred and ruptured membrane and cristae structures
Mitochondrial distribution	Perinuclear	Dispersed, mainly distributed in the cytoplasm of the cell
ATP production	Normal	Impaired
ROS generation	Normal	Increased
Fatty acid oxidation	Normal	Decreased
Mitochondrial membrane potential (MMP)	Normal	Decreased
Ca2+-induced mitochondrial permeability transition pore	Normal	Increased
NADH dehydrogenase activity	Normal	Decreased
Succinate dehydrogenase (SDH) activity	Normal	Decreased
Mitochondrial dynamics	Normal	Imbalance in mitochondrial fission and fusion
Mitochondrial biogenesis	Normal	Insufficient
Mitophagy	Normal	Transiently activated 3–7 days post-TAC, and downregulated thereafter