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  1. Article ; Online: Missing Causality and Heritability of Autoimmune Hepatitis.

    Czaja, Albert J

    Digestive diseases and sciences

    2022  Volume 68, Issue 4, Page(s) 1585–1604

    Abstract: ... inheritance of acquired epigenetic marks constitutes another mechanism of transmitting parental adaptations ... of acquired epigenetic marks. These unassessed or under-evaluated areas warrant investigation. ...

    Abstract Background: Autoimmune hepatitis has an unknown cause and genetic associations that are not disease-specific or always present. Clarification of its missing causality and heritability could improve prevention and management strategies.
    Aims: Describe the key epigenetic and genetic mechanisms that could account for missing causality and heritability in autoimmune hepatitis; indicate the prospects of these mechanisms as pivotal factors; and encourage investigations of their pathogenic role and therapeutic potential.
    Methods: English abstracts were identified in PubMed using multiple key search phases. Several hundred abstracts and 210 full-length articles were reviewed.
    Results: Environmental induction of epigenetic changes is the prime candidate for explaining the missing causality of autoimmune hepatitis. Environmental factors (diet, toxic exposures) can alter chromatin structure and the production of micro-ribonucleic acids that affect gene expression. Epistatic interaction between unsuspected genes is the prime candidate for explaining the missing heritability. The non-additive, interactive effects of multiple genes could enhance their impact on the propensity and phenotype of autoimmune hepatitis. Transgenerational inheritance of acquired epigenetic marks constitutes another mechanism of transmitting parental adaptations that could affect susceptibility. Management strategies could range from lifestyle adjustments and nutritional supplements to precision editing of the epigenetic landscape.
    Conclusions: Autoimmune hepatitis has a missing causality that might be explained by epigenetic changes induced by environmental factors and a missing heritability that might reflect epistatic gene interactions or transgenerational transmission of acquired epigenetic marks. These unassessed or under-evaluated areas warrant investigation.
    MeSH term(s) Humans ; Hepatitis, Autoimmune ; Epigenesis, Genetic ; Phenotype
    Language English
    Publishing date 2022-10-19
    Publishing country United States
    Document type Journal Article
    ZDB-ID 304250-9
    ISSN 1573-2568 ; 0163-2116
    ISSN (online) 1573-2568
    ISSN 0163-2116
    DOI 10.1007/s10620-022-07728-w
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  2. 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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  3. 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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  4. 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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  5. 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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  6. 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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  7. 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: ... increased markedly during acute liver injury from the hepatotoxin carbon tetrachloride. Serum levels ...

    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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  8. Article ; Online: Psychometric Properties of The Five-Item Victimization of Exploitation (FIVE) Scale: A Measure of Financial Abuse of Older Adults.

    Hancock, David W / Burnes, David P R / Pillemer, Karl A / Czaja, Sara J / Lachs, Mark S

    The Gerontologist

    2022  Volume 63, Issue 6, Page(s) 993–999

    Abstract: Background and objectives: Elder mistreatment affects at least 1 in 10 older adults. Financial abuse, or exploitation, of older adults is among the most commonly reported forms of abuse. Few validated measures exist to measure this construct. We aim to ... ...

    Abstract Background and objectives: Elder mistreatment affects at least 1 in 10 older adults. Financial abuse, or exploitation, of older adults is among the most commonly reported forms of abuse. Few validated measures exist to measure this construct. We aim to present a new psychometrically validated measure of financial abuse of older adults.
    Research design and methods: Classical test theory and item response theory (IRT) methodologies were used to examine a five-item measure of financial abuse of older adults, administered as part of the New York State Elder Mistreatment Survey.
    Results: Factor analysis revealed a single factor best fits the data, which we labeled as financial abuse. Moreover, IRT analyses revealed that these items discriminated well between abused and nonabused persons and provided information at high levels of the latent trait θ, as is expected in cases of abuse.
    Discussion and implications: The Five-Item Victimization of Exploitation Scale has acceptable psychometric properties and has been used successfully in large-scale survey research. We recommend this measure as an indicator of financial abuse in elder abuse, or mistreatment prevalence research studies.
    MeSH term(s) Humans ; Aged ; Psychometrics ; Elder Abuse ; New York ; Crime Victims ; Prevalence
    Language English
    Publishing date 2022-03-22
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 216760-8
    ISSN 1758-5341 ; 0016-9013
    ISSN (online) 1758-5341
    ISSN 0016-9013
    DOI 10.1093/geront/gnac048
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  9. 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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  10. Article ; Online: Epigenetic changes and their implications in autoimmune hepatitis.

    Czaja, Albert J

    European journal of clinical investigation

    2018  Volume 48, Issue 4

    Abstract: ... genes by marking messenger ribonucleic acids for degradation, and they can promote inflammatory activity ...

    Abstract Background: The genetic risk of autoimmune hepatitis is insufficient to explain the observed risk, and epigenetic changes may explain disparities in disease occurrence in different populations within and between countries. The goal of this review was to examine how epigenetic changes induced by the environment or inherited as a phenotypic trait may affect autoimmune hepatitis and be amenable to therapeutic intervention.
    Materials and methods: Pertinent abstracts were identified in PubMed by multiple search terms. The number of abstracts reviewed was 1689, and the number of full-length articles reviewed exceeded 150.
    Results: Activation of pro-inflammatory genes in autoimmune disease is associated with hypomethylation of deoxyribonucleic acid and modification of histones within chromatin. Organ-specific microribonucleic acids can silence genes by marking messenger ribonucleic acids for degradation, and they can promote inflammatory activity or immunosuppression. High circulating levels of the microribonucleic acids 21 and 122 have been demonstrated in autoimmune hepatitis, and they may increase production of pro-inflammatory cytokines. Microribonucleic acids are also essential for maintaining regulatory T cells. Drugs, pollutants, infections, diet and ageing can induce inheritable epigenetic changes favouring autoimmunity. Reversal is feasible by manipulating enzymes, transcription factors, gene-silencing molecules and toxic exposures or by administering methyl donors and correcting vitamin D deficiency. Gene targets, site specificity, efficacy and consequences are uncertain.
    Conclusions: Potentially reversible epigenetic changes may affect the occurrence and outcome of autoimmune hepatitis, and investigations are warranted to determine the nature of these changes, key genomic targets, and feasible interventions and their consequences.
    MeSH term(s) Autoimmunity/genetics ; DNA Methylation/genetics ; Environment ; Epigenesis, Genetic/genetics ; Gene-Environment Interaction ; Genes/genetics ; Hepatitis, Autoimmune/genetics ; Histone Code/genetics ; Humans ; MicroRNAs/genetics ; Promoter Regions, Genetic/genetics ; Transcription, Genetic/genetics
    Chemical Substances MicroRNAs
    Language English
    Publishing date 2018-02-18
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 186196-7
    ISSN 1365-2362 ; 0014-2972 ; 0960-135X
    ISSN (online) 1365-2362
    ISSN 0014-2972 ; 0960-135X
    DOI 10.1111/eci.12899
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