Disruption of Golgi apparatus homeostasis triggers cellular responses to maintain organelle function and protein balance. In this study, we found that an imbalance in Golgi proteins activates a novel pathway that transports specific Golgi proteins to lysosomes. This process is regulated by LRRK2 and its downstream effectors, Rab8 and Rab10, which are involved in membrane trafficking. Concurrently, we observed Golgi tubule formation, suggesting the development of transport intermediates. We also found that CAMSAP2, a microtubule minus-end binding protein that stabilizes Golgi-derived microtubules, clusters at the Golgi under stress conditions and may facilitate tubule formation for cargo transport. In addition, the appearance of LC3B on lysosomes under Golgi stress suggests activation of the conjugation of ATG8s to single membranes (CASM) pathway, which mediates the selective degradation of Golgi proteins. In summary, we identified a pathway in which Golgi membrane imbalance leads to LRRK2 and Rab activation, structural remodeling of the Golgi, CAMSAP2-dependent microtubule regulation, and selective degradation of Golgi proteins through CASM. This mechanism may represent an adaptive strategy that enables cells to resolve membrane stress and preserve organelle integrity.