**1. Introduction**

Mitochondria, considered as integral players in cellular energy production, represent a critical nexus of biological, psychological, and social factors underlying the mechanisms implicated in stress response. Oxidative stress is identified as an imbalance between the production of reactive oxygen species (ROS), including free radicals, and the antioxidant defense status in the living organisms. Free radicals are any atom or group of atoms containing one or more unpaired electrons in their outer valence shell, while ROS regroup all the free radicals and non-radical reactive species deriving from molecular oxygen and they are commonly found in biological systems [1]. As a result of their impaired ability for ATP synthesis and for an increased production of ROS, mitochondria appear to be central hubs of the pathophysiological process contributing to many diseases [2]. Mitochondria are especially abundant in the cardiac tissue; hence, mitochondrial dysregulation and ROS production are thought to contribute significantly to cardiac pathology. Cardiovascular diseases (CVD) are the leading cause of death in the world and oxidative stress is one of the most significant risk factors.

Under physiological conditions, cardiac ROS signaling regulates heart development and cardiomyocyte maturation, cardiac calcium handling, excitationcontraction coupling, and vascular tone [3]. However, pathological conditions of unregulated ROS production can result in oxidative stress, proteins and lipids damage and cell death [4]. It has been demonstrated that autophagy can be a crucial mechanism for preventing the accumulation of ROS by removing damaged mitochondria [5]. In this selective chapter, we will discuss the role of mitochondria in oxidative stress-related heart disorders.
