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  1. Article ; Online: Function of Autophagy in Nonalcoholic Fatty Liver Disease.

    Czaja, Mark J

    Digestive diseases and sciences

    2016  Volume 61, Issue 5, Page(s) 1304–1313

    Abstract: Autophagy is a lysosomal degradative pathway that functions to promote cell survival by supplying energy in times of stress or by removing damaged organelles and proteins after injury. The involvement of autophagy in the pathogenesis of nonalcoholic ... ...

    Abstract Autophagy is a lysosomal degradative pathway that functions to promote cell survival by supplying energy in times of stress or by removing damaged organelles and proteins after injury. The involvement of autophagy in the pathogenesis of nonalcoholic fatty liver disease (NAFLD) was first suggested by the finding that this pathway mediates the breakdown of intracellular lipids in hepatocytes and therefore may regulate the development of hepatic steatosis. Subsequent studies have demonstrated additional critical functions for autophagy in hepatocytes and other hepatic cell types such as macrophages and stellate cells that regulate insulin sensitivity, hepatocellular injury, innate immunity, fibrosis, and carcinogenesis. These findings suggest a number of possible mechanistic roles for autophagy in the development of NAFLD and progression to NASH and its complications. The functions of autophagy in the liver, together with findings of decreased hepatic autophagy in association with conditions that predispose to NAFLD such as obesity and aging, suggest that autophagy may be a novel therapeutic target in this disease.
    MeSH term(s) Autophagy/physiology ; Carcinoma, Hepatocellular/etiology ; Carcinoma, Hepatocellular/pathology ; Hepatocytes/metabolism ; Hepatocytes/pathology ; Humans ; Liver Neoplasms/etiology ; Liver Neoplasms/pathology ; Macrophages/physiology ; Non-alcoholic Fatty Liver Disease/complications ; Non-alcoholic Fatty Liver Disease/pathology
    Language English
    Publishing date 2016-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 304250-9
    ISSN 1573-2568 ; 0163-2116
    ISSN (online) 1573-2568
    ISSN 0163-2116
    DOI 10.1007/s10620-015-4025-x
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  2. Article ; Online: A new mechanism of lipotoxicity: Calcium channel blockers as a treatment for nonalcoholic steatohepatitis?

    Czaja, Mark J

    Hepatology (Baltimore, Md.)

    2015  Volume 62, Issue 1, Page(s) 312–314

    MeSH term(s) Animals ; Autophagy/physiology ; Calcium Channel Blockers/pharmacology ; Humans ; Lysosomes/metabolism ; Metabolic Diseases/drug therapy ; Obesity/complications ; Phagosomes/metabolism ; Verapamil/pharmacology
    Chemical Substances Calcium Channel Blockers ; Verapamil (CJ0O37KU29)
    Language English
    Publishing date 2015-07
    Publishing country United States
    Document type Comment ; Journal Article
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.27858
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  3. Article ; Online: A Novel Mechanism of Starvation-Stimulated Hepatic Autophagy: Calcium-Induced O-GlcNAc-Dependent Signaling.

    Shen, Yang / Czaja, Mark J

    Hepatology (Baltimore, Md.)

    2018  Volume 69, Issue 1, Page(s) 446–448

    MeSH term(s) Animals ; Autophagy ; Calcium Signaling ; Hepatocytes/physiology ; Mice ; N-Acetylglucosaminyltransferases/physiology ; Starvation
    Chemical Substances N-Acetylglucosaminyltransferases (EC 2.4.1.-) ; Ogt protein, mouse (EC 2.4.1.255)
    Language English
    Publishing date 2018-12-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.30118
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  4. Article ; Online: Oxidized Albumin-A Trojan Horse for p38 MAPK-Mediated Inflammation in Decompensated Cirrhosis.

    Cingolani, Francesca / Czaja, Mark J

    Hepatology (Baltimore, Md.)

    2018  Volume 68, Issue 5, Page(s) 1678–1680

    MeSH term(s) Albumins ; Cytokines ; Humans ; Inflammation ; Leukocytes ; Liver Cirrhosis ; p38 Mitogen-Activated Protein Kinases
    Chemical Substances Albumins ; Cytokines ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2018-10-11
    Publishing country United States
    Document type Editorial ; Periodical Index ; Comment
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.30164
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  5. Article ; Online: Reply: To PMID 23081825.

    Czaja, Mark J

    Hepatology (Baltimore, Md.)

    2013  Volume 58, Issue 2, Page(s) 831

    MeSH term(s) Adipose Tissue/pathology ; Aging/pathology ; Animals ; Diet, High-Fat/adverse effects ; Fatty Liver/pathology ; Humans ; Male
    Language English
    Publishing date 2013-08
    Publishing country United States
    Document type Comment ; Letter
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.26214
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  6. Article ; Online: Mouse liver injury induces hepatic macrophage FGF23 production.

    Kumar, Pradeep / Liu, Yunshan / Shen, Yang / Maher, Jacquelyn J / Cingolani, Francesca / Czaja, Mark J

    PloS one

    2022  Volume 17, Issue 3, Page(s) e0264743

    Abstract: Fibroblast growth factor 23 (FGF23) is a bone marrow cell produced hormone that functions in the intestine and kidney to regulate phosphate homeostasis. Increased serum FGF23 is a well-established predictor of mortality in renal disease, but recent ... ...

    Abstract Fibroblast growth factor 23 (FGF23) is a bone marrow cell produced hormone that functions in the intestine and kidney to regulate phosphate homeostasis. Increased serum FGF23 is a well-established predictor of mortality in renal disease, but recent findings linking increased levels to hepatic and cardiac diseases have suggested that other organs are sources of FGF23 or targets of its effects. The potential ability of the liver to produce FGF23 in response to hepatocellular injury was therefore examined. Very low levels of Fgf23 mRNA and FGF23 protein were detected in normal mouse liver, but the amounts increased markedly during acute liver injury from the hepatotoxin carbon tetrachloride. Serum levels of intact FGF23 were elevated during liver injury from carbon tetrachloride. Chronic liver injury induced by a high fat diet or elevated bile acids also increased hepatic FGF23 levels. Stimulation of toll-like receptor (TLR) 4-driven inflammation by gut-derived lipopolysaccharide (LPS) underlies many forms of liver injury, and LPS induced Fgf23 in the liver as well as in other organs. The LPS-inducible cytokines IL-1β and TNF increased hepatic Fgf23 expression as did a TLR2 agonist Pam2CSK3. Analysis of Fgf23 expression and FGF23 secretion in different hepatic cell types involved in liver injury identified the resident liver macrophage or Kupffer cell as a source of hepatic FGF23. LPS and cytokines selectively induced the hormone in these cells but not in hepatocytes or hepatic stellate cells. FGF23 failed to exert any autocrine effect on the inflammatory state of Kupffer cells but did trigger proinflammatory activation of hepatocytes. During liver injury inflammatory factors induce Kupffer cell production of FGF23 that may have a paracrine proinflammatory effect on hepatocytes. Liver-produced FGF23 may have systemic hormonal effects as well that influence diseases in in other organs.
    MeSH term(s) Animals ; Carbon Tetrachloride/pharmacology ; Cytokines/metabolism ; Fibroblast Growth Factors/metabolism ; Hepatocytes/metabolism ; Hormones/metabolism ; Kupffer Cells/metabolism ; Lipopolysaccharides/pharmacology ; Liver/metabolism ; Mice
    Chemical Substances Cytokines ; Hormones ; Lipopolysaccharides ; Fibroblast Growth Factors (62031-54-3) ; Carbon Tetrachloride (CL2T97X0V0)
    Language English
    Publishing date 2022-03-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2267670-3
    ISSN 1932-6203 ; 1932-6203
    ISSN (online) 1932-6203
    ISSN 1932-6203
    DOI 10.1371/journal.pone.0264743
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  7. Article ; Online: Inflammasome-mediated inflammation and fibrosis: It is more than just the IL-1β.

    Amir, Muhammad / Czaja, Mark J

    Hepatology (Baltimore, Md.)

    2017  Volume 67, Issue 2, Page(s) 479–481

    MeSH term(s) Animals ; Inflammasomes ; Inflammation ; Interleukin-17 ; Interleukin-1beta ; Liver ; Mice ; NLR Family, Pyrin Domain-Containing 3 Protein
    Chemical Substances Inflammasomes ; Interleukin-17 ; Interleukin-1beta ; NLR Family, Pyrin Domain-Containing 3 Protein ; Nlrp3 protein, mouse
    Language English
    Publishing date 2017-12-23
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.29491
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  8. Article ; Online: Functions of autophagy in hepatic and pancreatic physiology and disease.

    Czaja, Mark J

    Gastroenterology

    2011  Volume 140, Issue 7, Page(s) 1895–1908

    Abstract: Autophagy is a lysosomal pathway that degrades and recycles intracellular organelles and proteins to maintain energy homeostasis during times of nutrient deprivation and to remove damaged cell components. Recent studies have identified new functions for ... ...

    Abstract Autophagy is a lysosomal pathway that degrades and recycles intracellular organelles and proteins to maintain energy homeostasis during times of nutrient deprivation and to remove damaged cell components. Recent studies have identified new functions for autophagy under basal and stressed conditions. In the liver and pancreas, autophagy performs the standard functions of degrading mitochondria and aggregated proteins and regulating cell death. In addition, autophagy functions in these organs to regulate lipid accumulation in hepatic steatosis, trypsinogen activation in pancreatitis, and hepatitis virus replication. This review discusses the effects of autophagy on hepatic and pancreatic physiology and the contribution of this degradative process to diseases of these organs. The discovery of novel functions for this lysosomal pathway has increased our understanding of the pathophysiology of diseases in the liver and pancreas and suggested new possibilities for their treatment.
    MeSH term(s) Animals ; Autophagy ; Humans ; Liver/metabolism ; Liver/pathology ; Liver/physiopathology ; Liver Diseases/metabolism ; Liver Diseases/pathology ; Liver Diseases/physiopathology ; Lysosomes/metabolism ; Lysosomes/pathology ; Pancreas/metabolism ; Pancreas/pathology ; Pancreas/physiopathology ; Pancreatic Diseases/metabolism ; Pancreatic Diseases/pathology ; Pancreatic Diseases/physiopathology ; Signal Transduction
    Language English
    Publishing date 2011-04-23
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review ; Webcast
    ZDB-ID 80112-4
    ISSN 1528-0012 ; 0016-5085
    ISSN (online) 1528-0012
    ISSN 0016-5085
    DOI 10.1053/j.gastro.2011.04.038
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  9. Article ; Online: Two types of autophagy are better than one during hepatocyte oxidative stress.

    Czaja, Mark J

    Autophagy

    2011  Volume 7, Issue 1, Page(s) 96–97

    MeSH term(s) Animals ; Autophagy/drug effects ; Autophagy-Related Protein 5 ; Hepatocytes/drug effects ; Hepatocytes/enzymology ; Hepatocytes/pathology ; MAP Kinase Signaling System/drug effects ; Mice ; Mice, Knockout ; Microtubule-Associated Proteins/metabolism ; Mitochondria/drug effects ; Mitochondria/enzymology ; Models, Biological ; Molecular Chaperones/metabolism ; Oxidative Stress/drug effects ; Vitamin K 3/toxicity
    Chemical Substances Atg5 protein, mouse ; Autophagy-Related Protein 5 ; Microtubule-Associated Proteins ; Molecular Chaperones ; Vitamin K 3 (723JX6CXY5)
    Language English
    Publishing date 2011-01-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.4161/auto.7.1.13885
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  10. Article ; Online: Regulation and Functions of Autophagic Lipolysis.

    Cingolani, Francesca / Czaja, Mark J

    Trends in endocrinology and metabolism: TEM

    2016  Volume 27, Issue 10, Page(s) 696–705

    Abstract: The selective breakdown by autophagy of lipid droplet (LD)-stored lipids, termed lipophagy, is a lysosomal lipolytic pathway that complements the actions of cytosolic neutral lipases. The physiological importance of lipophagy has been demonstrated in ... ...

    Abstract The selective breakdown by autophagy of lipid droplet (LD)-stored lipids, termed lipophagy, is a lysosomal lipolytic pathway that complements the actions of cytosolic neutral lipases. The physiological importance of lipophagy has been demonstrated in multiple mammalian cell types, as well as in lower organisms, and this pathway has many functions in addition to supplying free fatty acids to maintain cellular energy stores. Recent studies have begun to delineate the molecular mechanisms of the selective recognition of LDs by the autophagic machinery, as well as the intricate crosstalk between the different forms of autophagy and neutral lipases. These studies have led to increased interest in the role of lipophagy in both human disease pathogenesis and therapy.
    Language English
    Publishing date 2016-10
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1042384-9
    ISSN 1879-3061 ; 1043-2760
    ISSN (online) 1879-3061
    ISSN 1043-2760
    DOI 10.1016/j.tem.2016.06.003
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