Atlastin-1 (ATL1) is a regulator of endoplasmic reticulum (ER) morphology, participating in tubular ER formation and protein synthesis. It has been implicated in the mTOR signaling pathway, which is crucial for various cellular processes such as cell growth, proliferation, and metabolism [1]. Mutations in ATL1 are known to be a causative factor for hereditary spastic paraplegia (HSP-ATL1, SPG3A), highlighting its importance in maintaining normal neuronal function [3,4,5,6].

In the context of pre-eclampsia, studies on HTR-8/SVneo cells have shown that ATL1 inhibits the proliferation and invasion of trophoblast cells via the inhibition of the mTOR signaling pathway. Down-regulation of ATL1 led to increased cell viability, proliferation, migration, and invasion, along with increased levels of p-p70S6K and p-mTOR, which are downstream effectors of the mTOR pathway. The mTOR inhibitor rapamycin reversed the promotive effect of siATL1 on cell proliferation, migration, and invasion [1]. In intracranial aneurysm research, silencing of circ-ATL1, a circular RNA related to ATL1, suppressed vascular smooth muscle cell (VSMC) migration, proliferation, and phenotypic modulation. SIRT5 and miR-455 were found to be downstream targets of circ-ATL1, and up-regulation of SIRT5 or inhibition of miR-455 reversed the inhibitory effects of circ-ATL1 silencing on VSMCs [2].

In conclusion, ATL1 plays a significant role in regulating cellular processes such as proliferation, invasion, and phenotypic modulation in various cell types. Its involvement in the mTOR signaling pathway and its association with diseases like pre-eclampsia and hereditary spastic paraplegia highlight its importance in both normal biological function and disease development. Studies on ATL1, including those using cell-based models, have provided valuable insights into the molecular mechanisms underlying these diseases, potentially paving the way for novel therapeutic strategies.