Atg5, short for autophagy related 5, is a key component in autophagy, a conserved intracellular degradative process. It is crucial for the formation of autophagosomes, a characteristic feature of autophagy. Atg5 binds with Atg12 and Atg16L1 to form an E3 like ligase complex necessary for autophagosome expansion. Autophagy, regulated by Atg5, plays a central role in maintaining cellular nutrient and energy homeostasis [2].

In Atg5 -deficient models, significant impacts are observed. In proximal tubule-specific autophagy-deficient mice, ablation of epithelial Atg5 genes impairs autophagy, leading to enhanced NF-κB activation, immune cell infiltration, and pro-inflammatory cytokines production in obstructed kidneys [1]. In male germ cell-specific Atg5-knockout mice, testicular autophagy activity decreases, resulting in reduced fertility, abnormal sperm development, and sperm individualization issues [3]. Myeloid cell-specific Atg5 knockout mice show reduced renal fibrosis and macrophage recruitment after certain kidney injuries, as Atg5 deficiency impairs the CCL20-CCR6 axis and inhibits M2 macrophage polarization [4].

In conclusion, Atg5 is essential for autophagy and has far-reaching impacts on multiple biological processes. Studies using Atg5 knockout or conditional knockout mouse models have revealed its role in inflammation-related diseases such as kidney inflammation, and in reproductive processes like male fertility. These models have significantly contributed to understanding Atg5's function in specific disease areas and biological processes.