Mitochondria are essential organelles in most eukaryotic cells, often described as the cell’s “powerhouse” due to their central role in energy production. They likely originated from bacteria through endosymbiosis and retain their own circular DNA, which is maternally inherited. Structurally, mitochondria consist of an outer membrane, an inter-membrane space, an inner membrane folded into cristae, and a matrix. The outer membrane is permeable due to porins, while the inner membrane is highly selective and rich in proteins that regulate transport and energy processes. The matrix contains enzymes, mitochondrial DNA, and ribosomes necessary for metabolic activity. Functionally, mitochondria are highly dynamic, capable of fission and fusion, and adapt their number and structure according to cellular energy demands. They play key roles in metabolic pathways such as the citric acid cycle, beta-oxidation of fatty acids, and parts of gluconeogenesis, urea cycle, and heme synthesis. Beyond metabolism, mitochondria are involved in calcium signaling, immune responses, steroid synthesis, and apoptosis, particularly through the release of cytochrome c. Dysfunction in mitochondrial components has been linked to diseases such as Parkinson’s and certain metabolic or genetic disorders. The primary function of mitochondria is ATP production through oxidative phosphorylation, which occurs across the inner membrane. Electrons from NADH and FADH₂ pass through the electron transport chain, driving proton pumping into the inter-membrane space and creating an electrochemical gradient. This gradient powers ATP synthase, which generates ATP as protons flow back into the matrix. Oxygen acts as the final electron acceptor, forming water. Disruption of this process—by toxins, genetic defects, or uncoupling mechanisms—can impair energy production, generate heat instead of ATP, or even lead to cell death.