Autophagy-Independent Functions of the Autophagy Machinery

Galluzzi, Lorenzo; Green, Douglas R.

doi:10.1016/j.cell.2019.05.026

Cited by 626 publications

(491 citation statements)

References 146 publications

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“…Beclin-1 is required in the pre-autophagosomal structure, and thus, its expression is associated with autophagosome activity. P62 is an autophagic degradation substrate, and a widely used marker of autophagic flux (Cirone et al, 2019;Galluzzi and Green, 2019). SCI recovery has been associated with autophagy (Kanno et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

Triptolide improves spinal cord injury by promoting autophagy and inhibiting apoptosis

Zhu

Ruan

Yang

et al. 2019

Cell Biology International

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We investigated the effect of triptolide (TP) on spinal cord injury (SCI), and its underlying mechanism. Following the establishment of the SCI model using YFP H‐line transgenic mice, TP was intraperitoneally injected at a dose of 0.2 mg/kg once daily for 7 days. Behavioral tests, Nissl staining, and hematoxylin–eosin staining were employed to assess motor function recovery and neuronal cell death. Western blot and immunofluorescence staining were used to assess autophagy‐associated proteins (LC3B, p62, Beclin‐1) and the apoptosis‐associated proteins (Bcl‐2, caspase‐3, Bax). The TP‐treated group showed improved motor functions, and reduced neuronal cell death. Also, significant upregulation of Bcl‐2 and LC3B expressions, with the downregulation of p62, Bax and caspase‐3 expressions were found in the TP‐treated group. Additionally, phosphorylation of extracellular signal‐regulated protein kinases 1 and 2 (ERK1 and ERK2) was decreased in the TP‐treated group. TP mediates its protective effect in SCI by promoting the autophagic pathway while inhibiting the MAPK/ERK1/2 signaling pathway. These results demonstrate the therapeutic potential of TP in SCI.

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Section: Discussionmentioning

confidence: 99%

Triptolide improves spinal cord injury by promoting autophagy and inhibiting apoptosis

Zhu

Ruan

Yang

et al. 2019

Cell Biology International

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“…These results suggest that the deficiency in cell migration does not arise from the progression and differentiation of the stem cell lineage. It has been recently reported that Atg5 deletion may produce an autophagy-independent effect (Galluzzi and Green, 2019). To verify this possibility, we genetically impaired the expression of Atg12, another essential autophagyrelated gene, using CRISPR/Cas9 technology.…”

Section: The Suppression Of Autophagy Hampers Cell Migration and Leadmentioning

confidence: 98%

The dynamic interplay between ATP/ADP levels and autophagy sustain neuronal migration in vivo

Bressan

Pecora

Gagnon

et al. 2020

Preprint

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Highlights ATP/ADP levels dynamically change during cell migration  A decrease in ATP levels leads to cell pausing and autophagy induction via AMPK  Autophagy is required to sustain neuronal migration by recycling focal adhesions  Autophagy level is dynamically modulated by migration-promoting and inhibiting cues AbstractCell migration is a dynamic process that entails extensive protein synthesis and recycling, structural remodeling, and a considerable bioenergetic demand. Autophagy is one of the pathways that maintain cellular homeostasis. Time-lapse imaging of autophagosomes and ATP/ADP levels in migrating cells in the rostral migratory stream of mice revealed that decrease in ATP levels force cells into the stationary phase and induce autophagy. Genetic impairment of autophagy in neuroblasts using either inducible conditional mice or CRISPR/Cas9 gene editing decreased cell migration due to the longer duration of the stationary phase. Autophagy is modulated in response to migration-promoting and inhibiting molecular cues and is required for the recycling of focal adhesions. Our results show that autophagy and energy consumption act in concert in migrating cells to dynamically regulate the pace and periodicity of the migratory and stationary phases in order to sustain neuronal migration.

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“…Nevertheless, depleting the essential autophagic vesicle protein ATG5 impairs MOPV, LASV, and JUNV replication [86][87][88], indicating that both OW and NW arenaviruses may utilize components of the autophagy pathway to aid in replication. While ATG5 is the key component in autophagy, there is increasing evidence that ATG5 also plays roles in non-autophagy processes, including negative regulation of RIG-I or MDA5 [89][90][91]. Thus, future studies are required to define if ATG5 is directly involved in arenavirus replication.…”

Section: Arenavirus Subversion Of Other Host Antiviral Defensesmentioning

confidence: 99%

Differential Immune Responses to Hemorrhagic Fever-Causing Arenaviruses

2019

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The family Arenaviridae contains several pathogens of major clinical importance. The Old World (OW) arenavirus Lassa virus is endemic in West Africa and is estimated to cause up to 300,000 infections each year. The New World (NW) arenaviruses Junín and Machupo periodically cause hemorrhagic fever outbreaks in South America. While these arenaviruses are highly pathogenic in humans, recent evidence indicates that pathogenic OW and NW arenaviruses interact with the host immune system differently, which may have differential impacts on viral pathogenesis. Severe Lassa fever cases are characterized by profound immunosuppression. In contrast, pathogenic NW arenavirus infections are accompanied by elevated levels of Type I interferon and pro-inflammatory cytokines. This review aims to summarize recent findings about interactions of these pathogenic arenaviruses with the innate immune machinery and the subsequent effects on adaptive immunity, which may inform the development of vaccines and therapeutics against arenavirus infections.

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Autophagy-Independent Functions of the Autophagy Machinery

Cited by 626 publications

References 146 publications

Triptolide improves spinal cord injury by promoting autophagy and inhibiting apoptosis

Triptolide improves spinal cord injury by promoting autophagy and inhibiting apoptosis

The dynamic interplay between ATP/ADP levels and autophagy sustain neuronal migration in vivo

Differential Immune Responses to Hemorrhagic Fever-Causing Arenaviruses

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