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Article: Effets hépatiques de l’alcool

Teixeira-Clerc, Fatima

Société française de nutrition Cahiers de nutrition et de diététique. 2015 Apr., v. 50, no. 2

2015

Abstract: Alcoholic liver disease is a leading cause of chronic liver disease and is responsible for a high morbidity and mortality. The spectrum of alcoholic liver disease includes steatosis, alcoholic hepatitis, fibrosis and its end-stage cirrhosis, and ... ...

Abstract	Alcoholic liver disease is a leading cause of chronic liver disease and is responsible for a high morbidity and mortality. The spectrum of alcoholic liver disease includes steatosis, alcoholic hepatitis, fibrosis and its end-stage cirrhosis, and hepatocellular carcinoma. Steatosis is defined by the accumulation of triglycerides in hepatocytes. Alcoholic hepatitis is characterized by the coexistence of steatosis, hepatocellular damage and inflammation. Repeated episodes of alcoholic hepatitis lead to activation of fibrogenesis mechanisms and to cirrhosis. Acute alcoholic hepatitis is a severe form of alcohol-related liver disease, characterized by an intense and prolonged inflammatory reaction associated with liver failure and a significant short-term mortality. The treatment of alcoholic hepatitis includes abstinence from alcohol, and corticosteroids in its severe form. However, despite an improvement of the short-term survival, the efficacy of the treatment remains inadequate. The development of new therapeutic approaches is therefore a major challenge. The processes underlying alcohol-induced liver injury are complex and not completely understood. However, in recent years, the mechanisms driving disease progression have been better defined owing to the use of numerous animal models. Thus, products of alcohol metabolism, oxidative stress, increased intestinal permeability to bacterial products and inflammation play a major role in the pathogenesis of alcoholic liver disease.
Keywords	adrenal cortex hormones ; alcoholic hepatitis ; alcohols ; animal models ; disease course ; fibrosis ; hepatocytes ; hepatoma ; inflammation ; liver ; liver failure ; metabolism ; morbidity ; mortality ; nutrition ; oxidative stress ; pathogenesis ; permeability ; therapeutics ; triacylglycerols
Language	English
Dates of publication	2015-04
Size	p. 94-102.
Publishing place	Elsevier Masson SAS
Document type	Article
ZDB-ID	840946-8
ISSN	0007-9960
ISSN	0007-9960
DOI	10.1016/j.cnd.2014.12.002
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Reply: To PMID 23728734.

Teixeira-Clerc, Fatima / Lotersztajn, Sophie

Hepatology (Baltimore, Md.)

2014 Volume 59, Issue 1, Page(s) 353–354

MeSH term(s)	Animals ; Female ; Heme Oxygenase-1/genetics ; Humans ; Liver Diseases, Alcoholic/genetics ; Male
Chemical Substances	Heme Oxygenase-1 (EC 1.14.14.18)
Language	English
Publishing date	2014-01
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	604603-4
ISSN	1527-3350 ; 0270-9139
ISSN (online)	1527-3350
ISSN	0270-9139
DOI	10.1002/hep.26533
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Article ; Online: The novel cyclophilin inhibitor C105SR reduces hepatic ischaemia-reperfusion injury via mitoprotection.

Kheyar, Amel / Ahnou, Nazim / Ahmed-Belkacem, Abdelhakim / Hulin, Anne / Pressiat, Claire / Ghaleh, Bijan / Guichou, Jean-François / Morin, Didier / Pawlotsky, Jean-Michel / Teixeira-Clerc, Fatima

JHEP reports : innovation in hepatology

2023 Volume 5, Issue 11, Page(s) 100876

Abstract: Background & aims: Mitochondrial permeability transition pore (mPTP) opening is critical for mediating cell death during hepatic ischaemia-reperfusion injury (IRI). Blocking mPTP opening by inhibiting cyclophilin D (CypD) is a promising pharmacological ... ...

Abstract	Background & aims: Mitochondrial permeability transition pore (mPTP) opening is critical for mediating cell death during hepatic ischaemia-reperfusion injury (IRI). Blocking mPTP opening by inhibiting cyclophilin D (CypD) is a promising pharmacological approach for the treatment of IRI. Here, we show that diastereoisomers of a new class of small-molecule cyclophilin inhibitors (SMCypIs) have properties that make them attractive candidates for the development of therapeutic agents against liver IRI. Methods: Derivatives of the parent SMCypI were synthesised and evaluated for their ability to inhibit CypD peptidyl-prolyl Results: The two compounds that showed the strongest inhibition of CypD PPIase activity and mPTP opening, C105 and C110, were selected. Their SR diastereoisomers carried the activity of the racemic mixture and exhibited mitoprotective properties superior to those of the known macrocyclic cyclophilin inhibitors cyclosporin A and alisporivir. C105SR was more potent than C110SR in inhibiting mPTP opening and prevented cell death in a model of hypoxia/reoxygenation. Finally, C105SR substantially protected against hepatic IRI Conclusions: We identified a novel cyclophilin inhibitor with strong mitoprotective properties both Impact and implications: Hepatic ischaemia-reperfusion injury (IRI) is one of the main causes of morbidity and mortality during or after liver surgery. However, no effective therapies are available to prevent or treat this devastating syndrome. An attractive strategy to prevent hepatic IRI aims at reducing cell death by targeting mitochondrial permeability transition pore opening, a phenomenon regulated by cyclophilin D. Here, we identified a new small-molecule cyclophilin inhibitor, and demonstrated the enhanced mitoprotective and hepatoprotective properties of one of its diastereoisomers both
Language	English
Publishing date	2023-08-16
Publishing country	Netherlands
Document type	Journal Article
ISSN	2589-5559
ISSN (online)	2589-5559
DOI	10.1016/j.jhepr.2023.100876
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Article ; Online: Tissue damage induces a conserved stress response that initiates quiescent muscle stem cell activation.

Machado, Léo / Geara, Perla / Camps, Jordi / Dos Santos, Matthieu / Teixeira-Clerc, Fatima / Van Herck, Jens / Varet, Hugo / Legendre, Rachel / Pawlotsky, Jean-Michel / Sampaolesi, Maurilio / Voet, Thierry / Maire, Pascal / Relaix, Frederic / Mourikis, Philippos

Cell stem cell

2021 Volume 28, Issue 6, Page(s) 1125–1135.e7

Abstract: Tissue damage dramatically alters how cells interact with their microenvironment. These changes in turn dictate cellular responses, such as stem cell activation, yet early cellular responses in vivo remain ill defined. We generated single-cell and ... ...

Abstract	Tissue damage dramatically alters how cells interact with their microenvironment. These changes in turn dictate cellular responses, such as stem cell activation, yet early cellular responses in vivo remain ill defined. We generated single-cell and nucleus atlases from intact, dissociated, and injured muscle and liver and identified a common stress response signature shared by multiple cell types across these organs. This prevalent stress response was detected in published datasets across a range of tissues, demonstrating high conservation but also a significant degree of data distortion in single-cell reference atlases. Using quiescent muscle stem cells as a paradigm of cell activation following injury, we captured early cell activation following muscle injury and found that an essential ERK1/2 primary proliferation signal precedes initiation of the Notch-regulated myogenic program. This study defines initial events in response to tissue perturbation and identifies a broadly conserved transcriptional stress response that acts in parallel with cell-specific adaptive alterations.
MeSH term(s)	Cell Proliferation ; Muscle Development ; Muscles ; Satellite Cells, Skeletal Muscle ; Stem Cells
Language	English
Publishing date	2021-02-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2375354-7
ISSN	1875-9777 ; 1934-5909
ISSN (online)	1875-9777
ISSN	1934-5909
DOI	10.1016/j.stem.2021.01.017
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Article ; Online: Macrophage autophagy protects against hepatocellular carcinogenesis in mice.

Deust, Anthony / Chobert, Marie-Noële / Demontant, Vanessa / Gricourt, Guillaume / Denaës, Timothé / Thiolat, Allan / Ruiz, Isaac / Rodriguez, Christophe / Pawlotsky, Jean-Michel / Teixeira-Clerc, Fatima

Scientific reports

2021 Volume 11, Issue 1, Page(s) 18809

Abstract: Autophagy is a lysosomal degradation pathway of cellular components that regulates macrophage properties. Macrophages are critically involved in tumor growth, metastasis, angiogenesis and immune suppression. Here, we investigated whether macrophage ... ...

Abstract	Autophagy is a lysosomal degradation pathway of cellular components that regulates macrophage properties. Macrophages are critically involved in tumor growth, metastasis, angiogenesis and immune suppression. Here, we investigated whether macrophage autophagy may protect against hepatocellular carcinoma (HCC). Experiments were performed in mice with deletion of the autophagy gene Atg5 in the myeloid lineage (ATG5
MeSH term(s)	Animals ; Autophagy ; Carcinoma, Hepatocellular/immunology ; Gene Expression Profiling ; Liver/metabolism ; Liver Neoplasms/immunology ; Macrophages/pathology ; Mice ; Mice, Knockout
Language	English
Publishing date	2021-09-22
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-98203-5
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Article ; Online: Cannabinoid signaling and liver therapeutics.

Mallat, Ariane / Teixeira-Clerc, Fatima / Lotersztajn, Sophie

Journal of hepatology

2013 Volume 59, Issue 4, Page(s) 891–896

Abstract: Over the last decade, the endocannabinoid system has emerged as a pivotal mediator of acute and chronic liver injury, with the description of the role of CB1 and CB2 receptors and their endogenous lipidic ligands in various aspects of liver ... ...

Abstract	Over the last decade, the endocannabinoid system has emerged as a pivotal mediator of acute and chronic liver injury, with the description of the role of CB1 and CB2 receptors and their endogenous lipidic ligands in various aspects of liver pathophysiology. A large number of studies have demonstrated that CB1 receptor antagonists represent an important therapeutic target, owing to beneficial effects on lipid metabolism and in light of its antifibrogenic properties. Unfortunately, the brain-penetrant CB1 antagonist rimonabant, initially approved for the management of overweight and related cardiometabolic risks, was withdrawn because of an alarming rate of mood adverse effects. However, the efficacy of peripherally-restricted CB1 antagonists with limited brain penetrance has now been validated in preclinical models of NAFLD, and beneficial effects on fibrosis and its complications are anticipated. CB2 receptor is currently considered as a promising anti-inflammatory and antifibrogenic target, although clinical development of CB2 agonists is still awaited. In this review, we highlight the latest advances on the impact of the endocannabinoid system on the key steps of chronic liver disease progression and discuss the therapeutic potential of molecules targeting cannabinoid receptors.
MeSH term(s)	Animals ; Apoptosis ; Endocannabinoids/metabolism ; Fatty Liver/metabolism ; Humans ; Liver Cirrhosis/metabolism ; Liver Diseases/drug therapy ; Liver Diseases/metabolism ; Liver Diseases/pathology ; Liver Diseases, Alcoholic/metabolism ; Liver Regeneration/physiology ; Non-alcoholic Fatty Liver Disease ; Receptor, Cannabinoid, CB1/antagonists & inhibitors ; Receptor, Cannabinoid, CB1/metabolism ; Receptor, Cannabinoid, CB2/agonists ; Receptor, Cannabinoid, CB2/metabolism ; Signal Transduction
Chemical Substances	Endocannabinoids ; Receptor, Cannabinoid, CB1 ; Receptor, Cannabinoid, CB2
Language	English
Publishing date	2013-10
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	605953-3
ISSN	1600-0641 ; 0168-8278
ISSN (online)	1600-0641
ISSN	0168-8278
DOI	10.1016/j.jhep.2013.03.032
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Article ; Online: Small-Molecule Inhibitors of Cyclophilins Block Opening of the Mitochondrial Permeability Transition Pore and Protect Mice From Hepatic Ischemia/Reperfusion Injury.

Panel, Mathieu / Ruiz, Isaac / Brillet, Rozenn / Lafdil, Fouad / Teixeira-Clerc, Fatima / Nguyen, Cong Trung / Calderaro, Julien / Gelin, Muriel / Allemand, Fred / Guichou, Jean-François / Ghaleh, Bijan / Ahmed-Belkacem, Abdelhakim / Morin, Didier / Pawlotsky, Jean-Michel

Gastroenterology

2019 Volume 157, Issue 5, Page(s) 1368–1382

Abstract: Background & aims: Hepatic ischemia/reperfusion injury is a complication of liver surgery that involves mitochondrial dysfunction resulting from mitochondrial permeability transition pore (mPTP) opening. Cyclophilin D (PPIF or CypD) is a peptidyl-prolyl ...

Abstract	Background & aims: Hepatic ischemia/reperfusion injury is a complication of liver surgery that involves mitochondrial dysfunction resulting from mitochondrial permeability transition pore (mPTP) opening. Cyclophilin D (PPIF or CypD) is a peptidyl-prolyl cis-trans isomerase that regulates mPTP opening in the inner mitochondrial membrane. We investigated whether and how recently created small-molecule inhibitors of CypD prevent opening of the mPTP in hepatocytes and the resulting effects in cell models and livers of mice undergoing ischemia/reperfusion injury. Methods: We measured the activity of 9 small-molecule inhibitors of cyclophilins in an assay of CypD activity. The effects of the small-molecule CypD inhibitors or vehicle on mPTP opening were assessed by measuring mitochondrial swelling and calcium retention in isolated liver mitochondria from C57BL/6J (wild-type) and Ppif Results: The compounds inhibited peptidyl-prolyl isomerase activity (half maximal inhibitory concentration values, 0.2-16.2 μmol/L) and, as a result, calcium-induced mitochondrial swelling, by preventing mPTP opening (half maximal inhibitory concentration values, 1.4-132 μmol/L) in a concentration-dependent manner. The most potent inhibitor (C31) bound CypD with high affinity and inhibited swelling in mitochondria from livers of wild-type and Ppif Conclusions: Recently created small-molecule inhibitors of CypD reduced calcium-induced swelling in mitochondria from mouse and human liver tissues. Administration of these compounds to mice during ischemia/reperfusion restored hepatic calcium retention capacity and oxidative phosphorylation parameters and reduced liver damage. These compounds might be developed to protect patients from ischemia/reperfusion injury after liver surgery or for other hepatic or nonhepatic disorders related to abnormal mPTP opening.
MeSH term(s)	Animals ; Calcium Signaling/drug effects ; Cells, Cultured ; Peptidyl-Prolyl Isomerase F/antagonists & inhibitors ; Peptidyl-Prolyl Isomerase F/genetics ; Peptidyl-Prolyl Isomerase F/metabolism ; Cytoprotection ; Disease Models, Animal ; Enzyme Inhibitors/pharmacology ; Humans ; Liver/drug effects ; Liver/enzymology ; Liver/pathology ; Liver Diseases/enzymology ; Liver Diseases/genetics ; Liver Diseases/pathology ; Liver Diseases/prevention & control ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondria, Liver/drug effects ; Mitochondria, Liver/enzymology ; Mitochondria, Liver/pathology ; Mitochondrial Membrane Transport Proteins/antagonists & inhibitors ; Mitochondrial Membrane Transport Proteins/metabolism ; Mitochondrial Permeability Transition Pore ; Mitochondrial Swelling/drug effects ; Reperfusion Injury/enzymology ; Reperfusion Injury/genetics ; Reperfusion Injury/pathology ; Reperfusion Injury/prevention & control ; Signal Transduction
Chemical Substances	Peptidyl-Prolyl Isomerase F ; Enzyme Inhibitors ; Mitochondrial Membrane Transport Proteins ; Mitochondrial Permeability Transition Pore ; PPIF protein, mouse
Language	English
Publishing date	2019-07-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80112-4
ISSN	1528-0012 ; 0016-5085
ISSN (online)	1528-0012
ISSN	0016-5085
DOI	10.1053/j.gastro.2019.07.026
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Article ; Online: Autophagy: a multifaceted partner in liver fibrosis.

Mallat, Ariane / Lodder, Jasper / Teixeira-Clerc, Fatima / Moreau, Richard / Codogno, Patrice / Lotersztajn, Sophie

BioMed research international

2014 Volume 2014, Page(s) 869390

Abstract: Liver fibrosis is a common wound healing response to chronic liver injury of all causes, and its end-stage cirrhosis is responsible for high morbidity and mortality worldwide. Fibrosis results from prolonged parenchymal cell apoptosis and necrosis ... ...

Abstract	Liver fibrosis is a common wound healing response to chronic liver injury of all causes, and its end-stage cirrhosis is responsible for high morbidity and mortality worldwide. Fibrosis results from prolonged parenchymal cell apoptosis and necrosis associated with an inflammatory reaction that leads to recruitment of immune cells, activation and accumulation of fibrogenic cells, and extracellular matrix accumulation. The fibrogenic process is driven by hepatic myofibroblasts, that mainly derive from hepatic stellate cells undergoing a transdifferentiation from a quiescent, lipid-rich into a fibrogenic myofibroblastic phenotype, in response to paracrine/autocrine signals produced by neighbouring inflammatory and parenchymal cells. Autophagy is an important regulator of liver homeostasis under physiological and pathological conditions. This review focuses on recent findings showing that autophagy is a novel, but complex, regulatory pathway in liver fibrosis, with profibrogenic effects relying on its direct contribution to the process of hepatic stellate cell activation, but with antifibrogenic properties via indirect hepatoprotective and anti-inflammatory properties. Therefore, cell-specific delivery of drugs that exploit autophagic pathways is a prerequisite to further consider autophagy as a potential target for antifibrotic therapy.
MeSH term(s)	Anti-Inflammatory Agents/therapeutic use ; Autophagy/drug effects ; Autophagy/genetics ; Cell Transdifferentiation/genetics ; Extracellular Matrix/metabolism ; Extracellular Matrix/pathology ; Hepatic Stellate Cells/drug effects ; Hepatic Stellate Cells/pathology ; Humans ; Inflammation/drug therapy ; Inflammation/metabolism ; Inflammation/pathology ; Liver/drug effects ; Liver/metabolism ; Liver/pathology ; Liver Cirrhosis/drug therapy ; Liver Cirrhosis/metabolism ; Liver Cirrhosis/pathology ; Myofibroblasts/drug effects ; Myofibroblasts/metabolism
Chemical Substances	Anti-Inflammatory Agents
Language	English
Publishing date	2014-08-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2698540-8
ISSN	2314-6141 ; 2314-6133
ISSN (online)	2314-6141
ISSN	2314-6133
DOI	10.1155/2014/869390
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Article ; Online: The Cannabinoid Receptor 2 Protects Against Alcoholic Liver Disease Via a Macrophage Autophagy-Dependent Pathway.

Denaës, Timothé / Lodder, Jasper / Chobert, Marie-Noële / Ruiz, Isaac / Pawlotsky, Jean-Michel / Lotersztajn, Sophie / Teixeira-Clerc, Fatima

Scientific reports

2016 Volume 6, Page(s) 28806

Abstract: Kupffer cells, the resident macrophages of the liver, play a major role in the pathogenesis of alcoholic liver disease. We have previously demonstrated that CB2 receptor protects against alcoholic liver disease by inhibiting alcohol-induced inflammation ... ...

Abstract	Kupffer cells, the resident macrophages of the liver, play a major role in the pathogenesis of alcoholic liver disease. We have previously demonstrated that CB2 receptor protects against alcoholic liver disease by inhibiting alcohol-induced inflammation and steatosis via the regulation of Kupffer cell activation. Here, we explored the mechanism underlying these effects and hypothesized that the anti-inflammatory properties of CB2 receptor in Kupffer cells rely on activation of autophagy. For this purpose, mice invalidated for CB2 receptor (CB2(Mye-/-) mice) or for the autophagy gene ATG5 (ATG5(Mye-/-) mice) in the myeloid lineage, and their littermate wild-type mice were subjected to chronic-plus-binge ethanol feeding. CB2(Mye-/-) mice showed exacerbated alcohol-induced pro-inflammatory gene expression and steatosis. Studies in cultured macrophages demonstrated that CB2 receptor activation by JWH-133 stimulated autophagy via a heme oxygenase-1 dependent pathway. Moreover, JWH-133 reduced the induction of inflammatory genes by lipopolysaccharide in wild-type macrophages, but not in ATG5-deficient cells. The CB2 agonist also protected from alcohol-induced liver inflammation and steatosis in wild-type mice, but not in ATG5(Mye-/-) mice demonstrating that macrophage autophagy mediates the anti-inflammatory and anti-steatogenic effects of CB2 receptor. Altogether these results demonstrate that CB2 receptor activation in macrophages protects from alcohol-induced steatosis by inhibiting hepatic inflammation through an autophagy-dependent pathway.
Language	English
Publishing date	2016-06-27
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/srep28806
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Article ; Online: Macrophage autophagy protects against liver fibrosis in mice.

Lodder, Jasper / Denaës, Timothé / Chobert, Marie-Noële / Wan, JingHong / El-Benna, Jamel / Pawlotsky, Jean-Michel / Lotersztajn, Sophie / Teixeira-Clerc, Fatima

Autophagy

2015 Volume 11, Issue 8, Page(s) 1280–1292

Abstract: Autophagy is a lysosomal degradation pathway of cellular components that displays antiinflammatory properties in macrophages. Macrophages are critically involved in chronic liver injury by releasing mediators that promote hepatocyte apoptosis, contribute ...

Abstract	Autophagy is a lysosomal degradation pathway of cellular components that displays antiinflammatory properties in macrophages. Macrophages are critically involved in chronic liver injury by releasing mediators that promote hepatocyte apoptosis, contribute to inflammatory cell recruitment and activation of hepatic fibrogenic cells. Here, we investigated whether macrophage autophagy may protect against chronic liver injury. Experiments were performed in mice with mutations in the autophagy gene Atg5 in the myeloid lineage (Atg5(fl/fl) LysM-Cre mice, referred to as atg5(-/-)) and their wild-type (Atg5(fl/fl), referred to as WT) littermates. Liver fibrosis was induced by repeated intraperitoneal injection of carbon tetrachloride. In vitro studies were performed in cultures or co-cultures of peritoneal macrophages with hepatic myofibroblasts. As compared to WT littermates, atg5(-/-) mice exposed to chronic carbon tetrachloride administration displayed higher hepatic levels of IL1A and IL1B and enhanced inflammatory cell recruitment associated with exacerbated liver injury. In addition, atg5(-/-) mice were more susceptible to liver fibrosis, as shown by enhanced matrix and fibrogenic cell accumulation. Macrophages from atg5(-/-) mice secreted higher levels of reactive oxygen species (ROS)-induced IL1A and IL1B. Moreover, hepatic myofibroblasts exposed to the conditioned medium of macrophages from atg5(-/-) mice showed increased profibrogenic gene expression; this effect was blunted when neutralizing IL1A and IL1B in the conditioned medium of atg5(-/-) macrophages. Finally, administration of recombinant IL1RN (interleukin 1 receptor antagonist) to carbon tetrachloride-exposed atg5(-/-) mice blunted liver injury and fibrosis, identifying IL1A/B as central mediators in the deleterious effects of macrophage autophagy invalidation. These results uncover macrophage autophagy as a novel antiinflammatory pathway regulating liver fibrosis.
MeSH term(s)	Animals ; Autophagy ; Autophagy-Related Protein 5 ; Carbon Tetrachloride/chemistry ; Cell Lineage ; Culture Media, Conditioned ; Disease Models, Animal ; Inflammation/metabolism ; Interleukin-1alpha/metabolism ; Interleukin-1beta/metabolism ; Kupffer Cells/cytology ; Liver/metabolism ; Liver/pathology ; Liver Cirrhosis/pathology ; Lysosomes/metabolism ; Macrophages/metabolism ; Macrophages/pathology ; Macrophages, Peritoneal/metabolism ; Mice ; Mice, Knockout ; Microtubule-Associated Proteins/genetics ; Microtubule-Associated Proteins/metabolism ; Mutation ; Myofibroblasts/metabolism ; Neutrophils/metabolism ; Reactive Oxygen Species/metabolism ; Recombinant Proteins/metabolism
Chemical Substances	Atg5 protein, mouse ; Autophagy-Related Protein 5 ; Culture Media, Conditioned ; IL1B protein, mouse ; Interleukin-1alpha ; Interleukin-1beta ; Microtubule-Associated Proteins ; Reactive Oxygen Species ; Recombinant Proteins ; Carbon Tetrachloride (CL2T97X0V0)
Language	English
Publishing date	2015
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2015.1058473
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