Energy flow through living systems is the focus of the biochemistry subfield known as bioenergetics. Transferring and converting energy is a topic of active biological research. It has uses in structural biology, mitochondrial metabolism, and diseases of that metabolism. The goal of the peer-reviewed, open-access Bioenergetics Journal is to publish the most thorough and trustworthy source of information on new findings and advancements in all fields of study through the publication of original articles, review articles, case studies, short communications, etc. and to make this information freely accessible online to researchers all over the world without any restrictions or additional subscriptions.

In the mitochondria, during cellular respiration (oxidative phosphorylation), a number of enzymes catalyse the transfer of electrons to molecule oxygen and the production of energy-storing adenosine triphosphate (ATP). Enzyme malfunctions that affect this pathway reduce cellular respiration and lower the ATP to ADP (adenosinediphosphate) ratio. Mitochondrial DNA [mtDNA], which comes from the mother, is unique to mitochondria. However, nuclear DNA and mtDNA both contribute to the operation of the mitochondria. Therefore, mitochondrial diseases can result from both nuclear and mitochondrial abnormalities. High energy-demanding tissues, such as the brain, nerves, retina, skeletal, and cardiac muscles, are particularly susceptible to oxidative phosphorylation abnormalities. Seizures, hypertonia, ophthalmoplegia, stroke-like episodes, muscle weakness, severe constipation, and cardiomyopathy are the most prevalent clinical symptoms. In mammalian cells, the electron transport chain is the principal oxygen consumer. From NADH and FADH2, the electron transport chain transfers electrons to protein complexes and mobile electron carriers. In the electron transport chain, cytochrome c and coenzyme Q are mobile electron carriers, and oxygen is the final electron acceptor. The malate and glycerol 3-phosphate shuttles also transfer reducing equivalents to the mitochondrial electron transport chain in addition to replenishing cytoplasmic NAD+ for glycolysis. Cellular respiration is stopped by oxidative phosphorylation inhibitors. Uncouplers separate oxidation from phosphorylation and assist animals in producing heat when they acclimate to the cold. Dysfunction of the respiratory chain is now widely acknowledged as a significant contributor to organ failure in human pathology. Due to its dual reliance on genes encoded by both nuclear and mitochondrial DNA (mtDNA), the biogenesis of the respiratory chain is unusual. Only 13 of the 100 respiratory chain subunits are encoded by the mtDNA, however these 13 subunits are crucial parts that are absolutely necessary for a functioning respiratory chain. Numerous hereditary disorders with respiratory chain malfunction brought on by mutations in genes with nuclear or mtDNA coding have been documented. Numerous hints point to a connection between mitochondrial malfunction and common conditions like heart failure, diabetes mellitus, neurodegeneration, and the ageing process. The clinically varied illnesses known as mitochondrial encephalomyopathies are grouped together because they are all caused by problems with the respiratory chain (oxidative phosphorylation [OXPHOS]). The final common metabolic process of mitochondrial energy metabolism, called oxidative phosphorylation, permits fatty acids, carbohydrates, and amino acids to be converted to water and carbon dioxide. Disorders of the nervous system and muscles can result from hereditary and environmental factors, such as medicines, impairing oxidative phosphorylation.