The update on transcriptional regulation of autophagy in normal and pathologic cells: A novel therapeutic target

Zhang, Zili; Guo, Mei; Zhao, Song; Xu, Wenxuan; Zhang, Feng; Wu, Liwei; Lu, Yin; Zheng, Shizhong

doi:10.1016/j.biopha.2015.06.003

Cited by 19 publications

(21 citation statements)

References 179 publications

(336 reference statements)

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“…3,6 Cytoplasmic FOXO3 levels were upregulated in CP tissues (Supplementary Figure F), in line with the possibility that BA-induced both FXR and FOXO3, which in turn attenuate autophagy activity in CP. In contrast, STAT3, which is another transcription factor that can inhibit autophagy signaling, 7 did not show any alteration in CP (data not shown). Quantitation values of FXR and autophagy are summarized in Table 2.…”

Section: Resultsmentioning

confidence: 89%

“…1,2 Similarly, nutritional and energy homeostasis is largely influenced by the evolutionarily conserved autophagy pathway. 3,4 Activation of FXR can suppress the activation of autophagy by diminishing the expression of several autophagy-related genes such as Atg7 and Lamp-2, 5,6,7 suggesting a link between BA, their action on FXR, autophagy and metabolic regulation. Autophagy is activated under cellular stress or upon energy depletion in order to sequester cytoplasmic components for their degradation/recycling and energy generation.…”

Section: Introductionmentioning

confidence: 99%

“…However, transcriptional regulators such as NFкB, FOXO3 and STAT3 can repress autophagy activity under different metabolic conditions. 7, 14,15,16,17, 18,19 Moreover, recent data indicate that autophagy also participates in the transcriptional regulation of a large numbers of genes that determine cellular energy status. 3 …”

Section: Introductionmentioning

confidence: 99%

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The bile acid receptor FXR attenuates acinar cell autophagy in chronic pancreatitis

et al. 2017

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The functional relationship between bile acid (BA) and autophagy has not been evaluated in the context of pancreatitis. Here we investigated whether BA and their nuclear farnesoid X receptor (FXR) modulate autophagy and the development of pancreatitis. FXR expression, autophagy, apoptosis and necroptosis were determined in human chronic pancreatitis (CP) tissue in vivo and in pancreatic cells lines in vitro by means of real-time PCR, immunoblots and immunofluorescence. Pancreatic cell lines exposed to the most abundant BAs glycochenodeoxycholate (GCDC) and taurocholic acid (TCA) increased the expression of nuclear FXR and diminished that of the essential autophagy-related protein ATG7. BA was also elevated in pancreatic tissues from CP patients, correlating with elevated FXR and curtailed ATG7 expression with locally reduced autophagic activity. This was accompanied by an increased manifestation of CP hallmarks including apoptosis, necroptosis, inflammation and fibrosis. The present results suggest a cascade of events in which local accumulation of BA signals via FXR to suppress autophagy in pancreatic acinar cells, thereby unleashing acinar cell apoptosis and necroptosis. Thus, BA may cause CP by suppressing autophagy and exacerbating acinar cell apoptosis and necroptosis.

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Section: Resultsmentioning

confidence: 89%

Section: Introductionmentioning

confidence: 99%

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The bile acid receptor FXR attenuates acinar cell autophagy in chronic pancreatitis

et al. 2017

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“…Owing to space limitations, this Cell Science at a Glance article can only act as an up-to-date introduction of this topic and is restricted to the mammalian system (for a more-detailed review see e.g. Pietrocola et al, 2013;Füllgrabe et al, 2014;Zhang et al, 2015). The work on transcription factors, such as TFEB, Jun and FOXO3, has shown us that the altered activity of a single transcription factor can be sufficient to either induce or inhibit autophagy.…”

Section: Perspectivesmentioning

confidence: 99%

Transcriptional regulation of mammalian autophagy at a glance

Füllgrabe

Ghislat

Cho

et al. 2016

Journal of Cell Science

170

171

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Macroautophagy, hereafter referred to as autophagy, is a catabolic process that results in the lysosomal degradation of cytoplasmic contents ranging from abnormal proteins to damaged cell organelles. It is activated under diverse conditions, including nutrient deprivation and hypoxia. During autophagy, members of the core autophagy-related (ATG) family of proteins mediate membrane rearrangements, which lead to the engulfment and degradation of cytoplasmic cargo. Recently, the nuclear regulation of autophagy, especially by transcription factors and histone modifiers, has gained increased attention. These factors are not only involved in rapid responses to autophagic stimuli, but also regulate the long-term outcome of autophagy. Now there are more than 20 transcription factors that have been shown to be linked to the autophagic process. However, their interplay and timing appear enigmatic as several have been individually shown to act as major regulators of autophagy. This Cell Science at a Glance article and the accompanying poster highlights the main cellular regulators of transcription involved in mammalian autophagy and their target genes.

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“…The longer-term transcriptional regulation of autophagy becomes further unravelled [51] and seems to be in favour of lipophagy. The transcription factor E" TFE" appears to be a master regulator of autophagy [5 ] and is involved in lipid metabolism as well.…”

Section: Autophagy As a Lipolytic Mechanismmentioning

confidence: 99%

Autophagy in Non-Alcoholic Fatty Liver Disease (NAFLD)

Kwanten¹,

Martinet²,

Francque³

2016

Autophagy in Current Trends in Cellular Physiology and Pathology

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Abstract"utophagy is a mechanism involved in cellular homeostasis under basal and stressed conditions delivering cytoplasmic content to the lysosomes for degradation to macronutrients. The potential role of autophagy in disease is increasingly recognised and investigated. To date, a key role of autophagy in hepatic lipid metabolism is recognised and dysfunctional autophagy might be an underlying cause of non-alcoholic faty liver disease N"FLD . Nevertheless, the exact role of autophagy in lipid metabolism remains controversial, with both a lipolytic function of autophagy and lipogenic function reported. This chapter aims to review the current knowledge on autophagy in N"FLD, with a special focus on its role in hepatic lipid metabolism, hepatic glucose metabolism and insulin resistance, steatohepatitis, hepatocellular injury and hepatic ibrogenesis. Finally, interaction with another cellular homeostatic process, the unfolded protein response UPR , will be briely discussed.

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The update on transcriptional regulation of autophagy in normal and pathologic cells: A novel therapeutic target

Cited by 19 publications

References 179 publications

The bile acid receptor FXR attenuates acinar cell autophagy in chronic pancreatitis

The bile acid receptor FXR attenuates acinar cell autophagy in chronic pancreatitis

Transcriptional regulation of mammalian autophagy at a glance

Autophagy in Non-Alcoholic Fatty Liver Disease (NAFLD)

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