Abstract: Introduction: One of the main events that regulate a cell’s well-being is cell-to-cell communication. This intercellular mechanism of information transfer is often mediated by vesicular trafficking. Mitochondrial-derived vesicles (MDVs) are an emerging subpopulation of extracellular vesicle (EV) first discovered in 2008 that allow mitochondria to communicate with their surroundings. The principal information and characteristics of these vesicles are proficiently discussed and summarized in a recent work published by Hazan Ben-Menachem et al. (2024). MDVs are vesicles ranging in size from 70 nm to 150 nm, originating from mitochondrial subcompartments and released into the cytosol. Depending on their biogenesis mechanism, they may present a single outer membrane or both an outer membrane and an inner membrane. Furthermore, they carry matrix proteins and oxidative phosphorylation system components (Hazan Ben-Menachem et al., 2024). These vesicles are capable of interacting with various intracellular organelles as well as the extracellular environment, producing EVs. This enables them to perform a dual role of transmitting intracellular signals and transporting mitochondrial components outside the cell. Accordingly, these vesicles remove damaged mitochondrial components, preserve mitochondrial structural and functional integrity, and restore proper homeostasis, thereby fulfilling a key role in mitochondrial quality control (Hazan Ben-Menachem et al., 2024). The formation of these MDVs is a housekeeping process that occurs physiologically in functionally active mitochondria. However, under pathological stress conditions, such as nutrient deprivation or exposure to toxins, and mitochondrial oxidative stress, their generation increases to remove damaged mitochondrial components. Interestingly, this process is beneficial for the cell and, although it shares several similarities, it is dissociated from mitophagy, which occurs later and only when the mitochondrion is severely damaged. Supporting this, MDV formation does not require autophagic machinery. Once assembled, the vesicles transporting mitochondria-damaged components move towards peroxisomes or lysosomes for degradation (Figure 1).