Mitochondrial dysfunctions related with oxidative stress

Mitochondria are central to ATP synthesis, regulation of Ca²⁺ homeostasis generation of reactive oxygen species and programmed cell death. They have an essential role in the generation of cell activation signals via released reactive species, as well as small GTPases; mitogen activated kinases located in the outer and inner membranes of mitochondria. While mutations of mitochondrial DNA leading to synthesis of malfunctional proteins are the most understood cause of cellular/organelle pathological changes, the mitochondrial dysfunction induced via oxidative damage to DNA, electron transport chain and structural proteins are also etiologically important events in development and progression in a wide array of diseases including malignancies, diabetes, hypertension, inflammation, hepatitis, neuromuscular and neurodegenerative ones. Although there is a growing amount of data regarding the mechanisms of mitochondrial dysfunction, one of the main challenges in the years to come will be to assess whether functional/structural modulation to mitochondrial proteins and damage to DNA is a cause or a consequence of disease. When mechanistic issues are sorted out, the use of mitochondria as a pharmacological target holds unforeseen promise in the treatment of diseases. Here we provide a short overview on newest discoveries supporting implication of mitochondria in inflammatory and apoptosis-based diseases.