Autophagy (self-eating) is an evolutionary process that removes damaged cellular proteins and organelles. When autophagy is induced, degrading cytoplasm and organelles are taken up into vesicles. . These vesicles are sent to the vacuolated or lysosomes in the yeast and mammalian cells, respectively. Provision of degradation of macromolecules and nutrient balance under stress conditions, such as starvation or oxidative stress or under normal conditions, is regulated by autophagy. In eukaryotic cells, autophagy is classified as macro-autophagy, micro-autophagy and chaperone-mediated autophagy according to the formation pattern. All of these promote the proteolytic degradation of cytosolic components in the lysosome and are regulated by autophage-linked genes and their associated enzymes. Macro-autophagy and micro-autophagy dependent lysosomal/vacuolar degradation processes are either non-selective or selective (selective). Chaperone-mediated autophagy is a selective autophagy used to reduce unfolded or misfolded cytosolic proteins. In the non-selective macro-autophagy, the cytoplasm is incorporated into the lysosome/vacuole by autophagosome, while in the micro-autophagy the soluble intracellular substrates are introduced into the lysosome/vacuole via tubular invaginations. The selective macro- or micro-autophagy target invasive microorganisms with various organelles that are either increased in number or damaged. In this case, autophagy is defined by special names such as reticulophagy or ERphagy, pexophagy, mitophagy, lipophagy, zimophagy, nucleophagy, ribophagy, aggrephagy and ksenophagy, according to the contents of the cargo. This review focuses on autophagy that functions as a cytoprotective program that destroys damaged organelles, protein deposits and intracellular pathogens in order to preserve the correct cellular functions.