The Golgi Apparatus May Be a Potential Therapeutic Target for Apoptosis-Related Neurological Diseases

Abstract

Increasing evidence shows that, in addition to the classical function of protein processing and transport, the Golgi apparatus (GA) is also involved in apoptosis, one of the most common forms of cell death. The structure and the function of the GA is damaged during apoptosis. However, the specific effect of the GA on the apoptosis process is unclear; it may be involved in initiating or promoting apoptosis, or it may inhibit apoptosis. Golgi-related apoptosis is associated with a variety of neurological diseases including glioma, Alzheimer's disease (AD), Parkinson's disease (PD), and ischemic stroke. This review summarizes the changes and the possible mechanisms of Golgi structure and function during apoptosis. In addition, we also explore the possible mechanisms by which the GA regulates apoptosis and summarize the potential relationship between the Golgi and certain neurological diseases from the perspective of apoptosis. Elucidation of the interaction between the GA and apoptosis broadens our understanding of the pathological mechanisms of neurological diseases and provides new research directions for the treatment of these diseases. Therefore, we propose that the GA may be a potential therapeutic target for apoptosis-related neurological diseases.

Orange-emissive carbon quantum dots for ligand-directed Golgi apparatus-targeting and in vivo imaging

“…Meanwhile, the abnormality of the Golgi apparatus can induce many diseases, such as Alzheimer's disease, Parkinson's disease, and various autoimmune diseases. 2,3 Therefore, it is necessary to design and develop a fluorescent probe that can accurately locate the Golgi apparatus for imaging and monitoring.…”

Disruption of Trip11 in cranial neural crest cells is associated with increased ER and Golgi stress contributing to skull defects in mice

“…To examine this possibility, expression of several Golgi stress markers was examined using control and Trip11 cKO skull tissues. Among analyzed Golgi stress markers, 24,[26][27][28] the expression levels of Golga2, Golgb1, Acbd3, Arf4, Cth, Slc7a1 and Slc7a11 were significantly increased in Trip11 cKO skulls compared with controls (Figure 7A). Western blot analysis further confirmed that the levels of GM130 (Golgi matrix protein 130, part of a cis-Golgi matrix protein) known as a marker of Golgi stress, 29 was increased in Trip11 cKO compared with wild-type skull (Figure 7B,C).…”

Illuminating Sub‐Cellular Organelles by Small Molecule AIEgens

“…[50,51] The morphological and functional changes in GA are implicated in diseases including cancer, neurodegeneration and cardiovascular disease. [52][53][54] To visualize the GA, Tang et al developed α-cyanostilbene based small molecule AIEgen (17, Figure 4a) which imaged GA in the HeLa cells as well as interacted with Cox-2 enzyme (Figure 4b). [39] In compound 17, the sulfoxamide group was used to target the sub-cellular GA in HeLa cells.…”

“…It works as the nodal point between exocytic and endocytic channels and helps in transporting different proteins into their destinations inside the cells [50,51] . The morphological and functional changes in GA are implicated in diseases including cancer, neurodegeneration and cardiovascular disease [52–54] . To visualize the GA, Tang et al .…”