Golgi Apparatus: A Potential Therapeutic Target for Autophagy-Associated Neurological Diseases

Abstract

Autophagy has dual effects in human diseases: appropriate autophagy may protect cells from stress, while excessive autophagy may cause cell death. Additionally, close interactions exist between autophagy and the Golgi. This review outlines recent advances regarding the role of the Golgi apparatus in autophagy. The signaling processes of autophagy are dependent on the normal function of the Golgi. Specifically, (i) autophagy-related protein 9 is mainly located in the Golgi and forms new autophagosomes in response to stressors; (ii) Golgi fragmentation is induced by Golgirelated proteins and accompanied with autophagy induction; and (iii) the endoplasmic reticulum-Golgi intermediate compartment and the reticular trans-Golgi network play essential roles in autophagosome formation to provide a template for lipidation of microtubule-associated protein 1A/1B-light chain 3 and induce further ubiquitination. Golgi-related proteins regulate formation of autophagosomes, and disrupted formation of autophagy can influence Golgi function. Notably, aberrant autophagy has been demonstrated to be implicated in neurological diseases. Thus, targeted therapies aimed at protecting the Golgi or regulating Golgi proteins might prevent or ameliorate autophagy-related neurological diseases. Further studies are needed to investigate the potential application of Golgi therapy in autophagy-based neurological diseases.

GOLGA2/GM130 is a novel target of neuroprotection therapy in intracerebral hemorrhage

“…As a signaling platform, the Golgi provides not only a membrane for autophagosome formation but also a location for induction and elongation of autophagosomes [15]. Moreover, Golgi-related proteins directly participate in autophagosome formation [15]. In our ICH in vivo models, LC3-II expression around the hematoma in the AAV-GM130 group was lower than that in the negative control group.…”

“…Autophagy can be in uenced by Golgi dysfunction. As a signaling platform, the Golgi provides not only a membrane for autophagosome formation but also a location for induction and elongation of autophagosomes [15]. Moreover, Golgi-related proteins directly participate in autophagosome formation [15].…”

“…Autophagy is usually enhanced under conditions of starvation, oxidative damage [13], endoplasmic reticulum stress [14] or Golgi stress [15]. Defects in autophagy ux may lead to the accumulation of damaged or aging proteins and play a critical role in the pathogenesis of several diseases, including neurodegenerative diseases [16], cardiovascular diseases [17], metabolic diseases [18], and cancer [19].…”

GOLGA2/GM130 is a Novel Target for Neuroprotection Therapy in Intracerebral Hemorrhage

“…Autophagy can be in uenced by Golgi dysfunction. As a signaling platform, the Golgi apparatus provides not only a membrane for autophagosome formation but also a location for autophagosome induction and elongation [15]. Additionally, Golgi-related proteins directly participate in autophagosome formation [15].…”

“…Autophagy is generally enhanced under conditions of starvation, oxidative damage [13], endoplasmic reticulum stress [14], or Golgi stress [15]. Defects in autophagic ux can lead to accumulation of damaged or aging proteins and thereby play a critical role in the pathogenesis of several diseases, including neurodegenerative diseases [16], cardiovascular diseases [17], metabolic diseases [18], and cancer [19].…”