Autosis occurs in the liver of patients with severe anorexia nervosa

Kheloufi, Marouane; Boulanger, Chantal M.; Codogno, Patrice; Rautou, Pierre‐Emmanuel

doi:10.1002/hep.27597

Cited by 38 publications

(21 citation statements)

References 10 publications

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“…Significantly, a small percentage of cells can be observed showing hallmarks of autosis in several models of nutrient starvation, i.e. starved cultured HeLa cells, neonatal rat hippocampal neurons following in vivo cerebral hypoxia-ischemia and the liver of anorexia-nervosa patients Kheloufi et al, 2015). Autosis is morphologically distinct from the ADCD described above, although it shares some features (Fig.…”

Section: Death From Autosismentioning

confidence: 85%

Autophagy-dependent cell death – where, how and why a cell eats itself to death

Bialik

Dasari

Kimchi

2018

Journal of Cell Science

246

165

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Autophagy as a means of cell killing was first advanced by Clark's phenotypic description of 'Type II autophagic cell death' in 1990. However, this phenomenon later came into question, because the presence of autophagosomes in dying cells does not necessarily signify that autophagy is the cause of demise, but rather may reflect the efforts of the cell to prevent it. Resolution of this issue comes from a more careful definition of autophagy-dependent cell death (ADCD) as a regulated cell death that is shown experimentally to require different components of the autophagy machinery without involvement of alternative cell death pathways. Following these strict criteria, ADCD has been validated in both lower model organisms and mammalian cells, highlighting its importance for developmental and pathophysiological cell death. Recently, researchers have defined additional morphological criteria that characterize ADCD and begun to explore how the established, well-studied autophagy pathway is subverted from a survival to a death function. This Review explores validated models of ADCD and focuses on the current understanding of the mechanisms by which autophagy can kill a cell.

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Section: Death From Autosismentioning

confidence: 85%

Autophagy-dependent cell death – where, how and why a cell eats itself to death

Bialik

Dasari

Kimchi

2018

Journal of Cell Science

246

165

View full text Add to dashboard Cite

show abstract

“…Fourth, strategies targeting a specific liver cell type using dedicated vectors would be highly desirable since they would likely limit side effects related to the physiological role of autophagy in all organs. Finally, defining careful dose adjustments and frequency of administration will be needed, since excessive activation of autophagy might be deleterious, 168 and therapeutic effects of autophagy-modulating agents might also be achieved with only intermittent therapy. 37 In addition, the circadian rhythm of autophagy in the liver is a parameter to be considered for optimization of treatment efficiency.…”

Section: Challenge For Translation Into Human Clinical Trialsmentioning

confidence: 99%

Autophagy in liver diseases: Time for translation?

Allaire

Rautou

Codogno

et al. 2019

Journal of Hepatology

Self Cite

307

222

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Autophagy is a self-eating catabolic pathway that contributes to liver homeostasis through its role in energy balance and in the quality control of the cytoplasm, by removing misfolded proteins, damaged organelles and lipid droplets. Autophagy not only regulates hepatocyte functions but also impacts on non-parenchymal cells, such as endothelial cells, macrophages and hepatic stellate cells. Deregulation of autophagy has been linked to many liver diseases and its modulation is now recognized as a potential new therapeutic strategy. Indeed, enhancing autophagy may prevent the progression of a number of liver diseases, including storage disorders (alpha-1 antitrypsin deficiency, Wilson's disease), acute liver injury, non-alcoholic steatohepatitis and chronic alcohol-related liver disease. Nevertheless, in some situations such as fibrosis, targeting specific liver cells must be considered, as autophagy displays opposing functions depending on the cell type. In addition, an optimal therapeutic time-window should be identified, since autophagy might be beneficial in the initial stages of disease, but detrimental at more advanced stages, as in the case of hepatocellular carcinoma. Finally, identifying biomarkers of autophagy and methods to monitor autophagic flux in vivo are important steps for the future development of personalized autophagy-targeting strategies. In this review, we provide an update on the regulatory role of autophagy in various aspects of liver pathophysiology, describing the different strategies to manipulate autophagy and discussing the potential to modulate autophagy as a therapeutic strategy in the context of liver diseases.

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“…Severely malnourished patients may suffer from hematological disorders and moderate to high increase of liver enzymes. The first pathophysiological changes are associated with bone marrow hypoplasia and with gelatinous marrow transformation [83,84]; the second seems to be multicausal and related to an ischemic hepatitis secondary to liver hypoperfusion, to oxidant stress from low glutathione levels, and to starvation-induced autophagy [83,85]. Both pathologies show a marked decrease after a few days during the replenishment phase (hydration and nutritional therapy) and possibly will normalize after the refeeding period [86].…”

Section: Important Clinical Sequelae Of Refeeding Syndrome and Managementioning

confidence: 99%

Management of Refeeding Syndrome in Medical Inpatients

Reber

Friedli

Vasiloglou

et al. 2019

JCM

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Refeeding syndrome (RFS) is the metabolic response to the switch from starvation to a fed state in the initial phase of nutritional therapy in patients who are severely malnourished or metabolically stressed due to severe illness. It is characterized by increased serum glucose, electrolyte disturbances (particularly hypophosphatemia, hypokalemia, and hypomagnesemia), vitamin depletion (especially vitamin B1 thiamine), fluid imbalance, and salt retention, with resulting impaired organ function and cardiac arrhythmias. The awareness of the medical and nursing staff is often too low in clinical practice, leading to under-diagnosis of this complication, which often has an unspecific clinical presentation. This review provides important insights into the RFS, practical recommendations for the management of RFS in the medical inpatient population (excluding eating disorders) based on consensus opinion and on current evidence from clinical studies, including risk stratification, prevention, diagnosis, and management and monitoring of nutritional and fluid therapy.confirmed RFS have significant mortality rates and increased non-elective hospital readmission, thus confirming the negative effect of RFS on clinical outcome [5,6].Nutritional treatment is a central aspect of modern multimodal inpatient therapy. It aims to reduce complications and mortality rates, and to improve patients' quality of life and autonomy [5,7]. Even though well tolerated, nutritional treatment has a potential risk of complications, including RFS, which is an exacerbated response to the metabolic change from a starvation to a fed state as a consequence of large amount of food in the replenishment phase. RFS is characterized by an imbalance of electrolytes (mainly phosphate, potassium, and magnesium), vitamin disturbances (e.g., vitamin B1 thiamine deficiency), and fluid imbalances, as well as limited organ functions, in some cases leading to mortality [8][9][10][11][12]. This article highlights, discusses, and reviews RFS in medical inpatients (excluding patients with eating disorders) in terms of pathophysiological aspects, preventive measures, clinical manifestations, risk evaluation, diagnostic procedures, and treatment methods.

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Autosis occurs in the liver of patients with severe anorexia nervosa

Cited by 38 publications

References 10 publications

Autophagy-dependent cell death – where, how and why a cell eats itself to death

Autophagy-dependent cell death – where, how and why a cell eats itself to death

Autophagy in liver diseases: Time for translation?

Management of Refeeding Syndrome in Medical Inpatients

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