Autophagy, a cellular self-degradation system, plays a crucial role in extending longevity. As organisms age, the activity of autophagy declines, primarily due to the increase of an inhibitory factor called Rubicon. This increase has been observed in various organisms such as nematodes, fruit flies, and mice. Activating autophagy has shown promising effects on lifespan extension. For instance, inhibiting Rubicon in model organisms like nematodes and fruit flies has resulted in increased lifespan. In mice, enhanced autophagy has improved age-related conditions and reduced cellular senescence. Research has identified several mechanisms to activate autophagy, including the suppression of Rubicon, the action of the transcription factor MondoA, and mutations in Beclin 1 that disrupt its binding with BCL2 protein, leading to increased autophagy and extended lifespan in mice. The potential of autophagy activation holds promise for extending healthy lifespan and treating age-related diseases. Future developments may focus on targeted therapies involving Rubicon and other autophagy-related factors, as well as drugs that enhance autophagy, paving the way for significant advancements in health and longevity.