Advanced Search
Display options
Filter resources
Text Availability
Article type
Publication date
Species
Language
Sex
Age
Showing 1 to 12 of 62 entries
Sorted by: Best Match Show Resources per page
Glutathione and mitochondria.

Frontiers in pharmacology

Ribas V, García-Ruiz C, Fernández-Checa JC.
PMID: 25024695
Front Pharmacol. 2014 Jul 01;5:151. doi: 10.3389/fphar.2014.00151. eCollection 2014.

Glutathione (GSH) is the main non-protein thiol in cells whose functions are dependent on the redox-active thiol of its cysteine moiety that serves as a cofactor for a number of antioxidant and detoxifying enzymes. While synthesized exclusively in the...

Cite
Ribas V, García-Ruiz C, Fernández-Checa JC. Glutathione and mitochondria. Front Pharmacol. 2014;5:151doi: 10.3389/fphar.2014.00151.
Ribas, V., García-Ruiz, C., & Fernández-Checa, J. C. (2014). Glutathione and mitochondria. Frontiers in pharmacology, 5151. https://doi.org/10.3389/fphar.2014.00151
Ribas, Vicent, et al. "Glutathione and mitochondria." Frontiers in pharmacology vol. 5 (2014): 151. doi: https://doi.org/10.3389/fphar.2014.00151
Ribas V, García-Ruiz C, Fernández-Checa JC. Glutathione and mitochondria. Front Pharmacol. 2014 Jul 01;5:151. doi: 10.3389/fphar.2014.00151. eCollection 2014. PMID: 25024695; PMCID: PMC4079069.
Copy Download .nbib Format: NLM
Gene expression modifications in the liver caused by binge drinking and S-adenosylmethionine feeding. The role of epigenetic changes.

Genes & nutrition

Li J, Bardag-Gorce F, Oliva J, Dedes J, French BA, French SW.
PMID: 19960281
Genes Nutr. 2010 Jun;5(2):169-79. doi: 10.1007/s12263-009-0158-x. Epub 2009 Dec 04.

Chronic ethanol ingestion, achieved by feeding ethanol at a constant rate using intragastric tube feeding, alters the expression of genes in the liver. This is done by epigenetic mechanisms, which depend on the blood alcohol levels at the time...

Cite
Li J, Bardag-Gorce F, Oliva J, et al. Gene expression modifications in the liver caused by binge drinking and S-adenosylmethionine feeding. The role of epigenetic changes. Genes Nutr. 2009;5(2):169-79doi: 10.1007/s12263-009-0158-x.
Li, J., Bardag-Gorce, F., Oliva, J., Dedes, J., French, B. A., & French, S. W. (2010). Gene expression modifications in the liver caused by binge drinking and S-adenosylmethionine feeding. The role of epigenetic changes. Genes & nutrition, 5(2), 169-79. https://doi.org/10.1007/s12263-009-0158-x
Li, Jun, et al. "Gene expression modifications in the liver caused by binge drinking and S-adenosylmethionine feeding. The role of epigenetic changes." Genes & nutrition vol. 5,2 (2010): 169-79. doi: https://doi.org/10.1007/s12263-009-0158-x
Li J, Bardag-Gorce F, Oliva J, Dedes J, French BA, French SW. Gene expression modifications in the liver caused by binge drinking and S-adenosylmethionine feeding. The role of epigenetic changes. Genes Nutr. 2010 Jun;5(2):169-79. doi: 10.1007/s12263-009-0158-x. Epub 2009 Dec 04. PMID: 19960281; PMCID: PMC2885163.
Copy Download .nbib Format: NLM
Cell signals influencing hepatic fibrosis.

International journal of hepatology

Cong M, Iwaisako K, Jiang C, Kisseleva T.
PMID: 22973518
Int J Hepatol. 2012;2012:158547. doi: 10.1155/2012/158547. Epub 2012 Aug 29.

Liver fibrosis is the result of the entire organism responding to a chronic injury. Every cell type in the liver contributes to the fibrosis. This paper first discusses key intracellular signaling pathways that are induced during liver fibrosis. The...

Cite
Cong M, Iwaisako K, Jiang C, et al. Cell signals influencing hepatic fibrosis. Int J Hepatol. 2012;2012:158547doi: 10.1155/2012/158547.
Cong, M., Iwaisako, K., Jiang, C., & Kisseleva, T. (2012). Cell signals influencing hepatic fibrosis. International journal of hepatology, 2012158547. https://doi.org/10.1155/2012/158547
Cong, Min, et al. "Cell signals influencing hepatic fibrosis." International journal of hepatology vol. 2012 (2012): 158547. doi: https://doi.org/10.1155/2012/158547
Cong M, Iwaisako K, Jiang C, Kisseleva T. Cell signals influencing hepatic fibrosis. Int J Hepatol. 2012;2012:158547. doi: 10.1155/2012/158547. Epub 2012 Aug 29. PMID: 22973518; PMCID: PMC3437636.
Copy Download .nbib Format: NLM
The gut-liver axis and the intersection with the microbiome.

Nature reviews. Gastroenterology & hepatology

Tripathi A, Debelius J, Brenner DA, Karin M, Loomba R, Schnabl B, Knight R.
PMID: 29748586
Nat Rev Gastroenterol Hepatol. 2018 Jul;15(7):397-411. doi: 10.1038/s41575-018-0011-z.

In the past decade, an exciting realization has been that diverse liver diseases - ranging from nonalcoholic steatohepatitis, alcoholic steatohepatitis and cirrhosis to hepatocellular carcinoma - fall along a spectrum. Work on the biology of the gut-liver axis has...

Cite
Tripathi A, Debelius J, Brenner DA, et al. The gut-liver axis and the intersection with the microbiome. Nat Rev Gastroenterol Hepatol. 2018;15(7):397-411doi: 10.1038/s41575-018-0011-z.
Tripathi, A., Debelius, J., Brenner, D. A., Karin, M., Loomba, R., Schnabl, B., & Knight, R. (2018). The gut-liver axis and the intersection with the microbiome. Nature reviews. Gastroenterology & hepatology, 15(7), 397-411. https://doi.org/10.1038/s41575-018-0011-z
Tripathi, Anupriya, et al. "The gut-liver axis and the intersection with the microbiome." Nature reviews. Gastroenterology & hepatology vol. 15,7 (2018): 397-411. doi: https://doi.org/10.1038/s41575-018-0011-z
Tripathi A, Debelius J, Brenner DA, Karin M, Loomba R, Schnabl B, Knight R. The gut-liver axis and the intersection with the microbiome. Nat Rev Gastroenterol Hepatol. 2018 Jul;15(7):397-411. doi: 10.1038/s41575-018-0011-z. PMID: 29748586; PMCID: PMC6319369.
Copy Download .nbib Format: NLM
Novel Small Molecule Inhibitors of Protein Kinase D Suppress NF-kappaB Activation and Attenuate the Severity of Rat Cerulein Pancreatitis.

Frontiers in physiology

Yuan J, Tan T, Geng M, Tan G, Chheda C, Pandol SJ.
PMID: 29270134
Front Physiol. 2017 Dec 07;8:1014. doi: 10.3389/fphys.2017.01014. eCollection 2017.

Nuclear factor-kappa B (NF-κB) activation is a key early signal regulating inflammatory and cell death responses in acute pancreatitis. Our previous

Cite
Yuan J, Tan T, Geng M, et al. Novel Small Molecule Inhibitors of Protein Kinase D Suppress NF-kappaB Activation and Attenuate the Severity of Rat Cerulein Pancreatitis. Front Physiol. 2017;8:1014doi: 10.3389/fphys.2017.01014.
Yuan, J., Tan, T., Geng, M., Tan, G., Chheda, C., & Pandol, S. J. (2017). Novel Small Molecule Inhibitors of Protein Kinase D Suppress NF-kappaB Activation and Attenuate the Severity of Rat Cerulein Pancreatitis. Frontiers in physiology, 81014. https://doi.org/10.3389/fphys.2017.01014
Yuan, Jingzhen, et al. "Novel Small Molecule Inhibitors of Protein Kinase D Suppress NF-kappaB Activation and Attenuate the Severity of Rat Cerulein Pancreatitis." Frontiers in physiology vol. 8 (2017): 1014. doi: https://doi.org/10.3389/fphys.2017.01014
Yuan J, Tan T, Geng M, Tan G, Chheda C, Pandol SJ. Novel Small Molecule Inhibitors of Protein Kinase D Suppress NF-kappaB Activation and Attenuate the Severity of Rat Cerulein Pancreatitis. Front Physiol. 2017 Dec 07;8:1014. doi: 10.3389/fphys.2017.01014. eCollection 2017. PMID: 29270134; PMCID: PMC5725929.
Copy Download .nbib Format: NLM
Ethanol Induced Disordering of Pancreatic Acinar Cell Endoplasmic Reticulum: An ER Stress/Defective Unfolded Protein Response Model.

Cellular and molecular gastroenterology and hepatology

Waldron RT, Su HY, Piplani H, Capri J, Cohn W, Whitelegge JP, Faull KF, Sakkiah S, Abrol R, Yang W, Zhou B, Freeman MR, Pandol SJ, Lugea A.
PMID: 29930975
Cell Mol Gastroenterol Hepatol. 2018 Jan 06;5(4):479-497. doi: 10.1016/j.jcmgh.2018.01.001. eCollection 2018.

BACKGROUND & AIMS: Heavy alcohol drinking is associated with pancreatitis, whereas moderate intake lowers the risk. Mice fed ethanol long term show no pancreas damage unless adaptive/protective responses mediating proteostasis are disrupted. Pancreatic acini synthesize digestive enzymes (largely serine...

Cite
Waldron RT, Su HY, Piplani H, et al. Ethanol Induced Disordering of Pancreatic Acinar Cell Endoplasmic Reticulum: An ER Stress/Defective Unfolded Protein Response Model. Cell Mol Gastroenterol Hepatol. 2018;5(4):479-497doi: 10.1016/j.jcmgh.2018.01.001.
Waldron, R. T., Su, H. Y., Piplani, H., Capri, J., Cohn, W., Whitelegge, J. P., Faull, K. F., Sakkiah, S., Abrol, R., Yang, W., Zhou, B., Freeman, M. R., Pandol, S. J., & Lugea, A. (2018). Ethanol Induced Disordering of Pancreatic Acinar Cell Endoplasmic Reticulum: An ER Stress/Defective Unfolded Protein Response Model. Cellular and molecular gastroenterology and hepatology, 5(4), 479-497. https://doi.org/10.1016/j.jcmgh.2018.01.001
Waldron, Richard T, et al. "Ethanol Induced Disordering of Pancreatic Acinar Cell Endoplasmic Reticulum: An ER Stress/Defective Unfolded Protein Response Model." Cellular and molecular gastroenterology and hepatology vol. 5,4 (2018): 479-497. doi: https://doi.org/10.1016/j.jcmgh.2018.01.001
Waldron RT, Su HY, Piplani H, Capri J, Cohn W, Whitelegge JP, Faull KF, Sakkiah S, Abrol R, Yang W, Zhou B, Freeman MR, Pandol SJ, Lugea A. Ethanol Induced Disordering of Pancreatic Acinar Cell Endoplasmic Reticulum: An ER Stress/Defective Unfolded Protein Response Model. Cell Mol Gastroenterol Hepatol. 2018 Jan 06;5(4):479-497. doi: 10.1016/j.jcmgh.2018.01.001. eCollection 2018. PMID: 29930975; PMCID: PMC6009017.
Copy Download .nbib Format: NLM
Heterogeneity of HSCs in a Mouse Model of NASH.

Hepatology (Baltimore, Md.)

Rosenthal SB, Liu X, Ganguly S, Dhar D, Pasillas MP, Ricciardelli E, Li RZ, Troutman TD, Kisseleva T, Glass CK, Brenner DA.
PMID: 33550587
Hepatology. 2021 Aug;74(2):667-685. doi: 10.1002/hep.31743. Epub 2021 Aug 10.

BACKGROUND AND AIMS: In clinical and experimental NASH, the origin of the scar-forming myofibroblast is the HSC. We used foz/foz mice on a Western diet to characterize in detail the phenotypic changes of HSCs in a NASH model.APPROACH AND...

Cite
Rosenthal SB, Liu X, Ganguly S, et al. Heterogeneity of HSCs in a Mouse Model of NASH. Hepatology. 2021;74(2):667-685doi: 10.1002/hep.31743.
Rosenthal, S. B., Liu, X., Ganguly, S., Dhar, D., Pasillas, M. P., Ricciardelli, E., Li, R. Z., Troutman, T. D., Kisseleva, T., Glass, C. K., & Brenner, D. A. (2021). Heterogeneity of HSCs in a Mouse Model of NASH. Hepatology (Baltimore, Md.), 74(2), 667-685. https://doi.org/10.1002/hep.31743
Rosenthal, Sara Brin, et al. "Heterogeneity of HSCs in a Mouse Model of NASH." Hepatology (Baltimore, Md.) vol. 74,2 (2021): 667-685. doi: https://doi.org/10.1002/hep.31743
Rosenthal SB, Liu X, Ganguly S, Dhar D, Pasillas MP, Ricciardelli E, Li RZ, Troutman TD, Kisseleva T, Glass CK, Brenner DA. Heterogeneity of HSCs in a Mouse Model of NASH. Hepatology. 2021 Aug;74(2):667-685. doi: 10.1002/hep.31743. Epub 2021 Aug 10. PMID: 33550587; PMCID: PMC8346581.
Copy Download .nbib Format: NLM
The gut mycobiome: a novel player in chronic liver diseases.

Journal of gastroenterology

Jiang L, Stärkel P, Fan JG, Fouts DE, Bacher P, Schnabl B.
PMID: 33151407
J Gastroenterol. 2021 Jan;56(1):1-11. doi: 10.1007/s00535-020-01740-5. Epub 2020 Nov 05.

The human gut microbiome (bacteria, fungi, viruses, and archaea) is a complex and diverse ecosystem. It plays an important role in human health, but is involved in several intestinal and extraintestinal diseases. Most research to date has focused on...

Cite
Jiang L, Stärkel P, Fan JG, et al. The gut mycobiome: a novel player in chronic liver diseases. J Gastroenterol. 2020;56(1):1-11doi: 10.1007/s00535-020-01740-5.
Jiang, L., Stärkel, P., Fan, J. G., Fouts, D. E., Bacher, P., & Schnabl, B. (2021). The gut mycobiome: a novel player in chronic liver diseases. Journal of gastroenterology, 56(1), 1-11. https://doi.org/10.1007/s00535-020-01740-5
Jiang, Lu, et al. "The gut mycobiome: a novel player in chronic liver diseases." Journal of gastroenterology vol. 56,1 (2021): 1-11. doi: https://doi.org/10.1007/s00535-020-01740-5
Jiang L, Stärkel P, Fan JG, Fouts DE, Bacher P, Schnabl B. The gut mycobiome: a novel player in chronic liver diseases. J Gastroenterol. 2021 Jan;56(1):1-11. doi: 10.1007/s00535-020-01740-5. Epub 2020 Nov 05. PMID: 33151407; PMCID: PMC7819863.
Copy Download .nbib Format: NLM
Contribution of bone marrow-derived fibrocytes to liver fibrosis.

Hepatobiliary surgery and nutrition

Xu J, Cong M, Park TJ, Scholten D, Brenner DA, Kisseleva T.
PMID: 25713803
Hepatobiliary Surg Nutr. 2015 Feb;4(1):34-47. doi: 10.3978/j.issn.2304-3881.2015.01.01.

Since the discovery of fibrocytes in 1994 by Dr. Bucala and colleagues, these bone marrow (BM)-derived collagen Type I producing CD45(+) cells remain the most fascinating cells of the hematopoietic system. Despite recent reports on the emerging contribution of...

Cite
Xu J, Cong M, Park TJ, et al. Contribution of bone marrow-derived fibrocytes to liver fibrosis. Hepatobiliary Surg Nutr. 2015;4(1):34-47doi: 10.3978/j.issn.2304-3881.2015.01.01.
Xu, J., Cong, M., Park, T. J., Scholten, D., Brenner, D. A., & Kisseleva, T. (2015). Contribution of bone marrow-derived fibrocytes to liver fibrosis. Hepatobiliary surgery and nutrition, 4(1), 34-47. https://doi.org/10.3978/j.issn.2304-3881.2015.01.01
Xu, Jun, et al. "Contribution of bone marrow-derived fibrocytes to liver fibrosis." Hepatobiliary surgery and nutrition vol. 4,1 (2015): 34-47. doi: https://doi.org/10.3978/j.issn.2304-3881.2015.01.01
Xu J, Cong M, Park TJ, Scholten D, Brenner DA, Kisseleva T. Contribution of bone marrow-derived fibrocytes to liver fibrosis. Hepatobiliary Surg Nutr. 2015 Feb;4(1):34-47. doi: 10.3978/j.issn.2304-3881.2015.01.01. PMID: 25713803; PMCID: PMC4318956.
Copy Download .nbib Format: NLM
Advanced preclinical models for evaluation of drug-induced liver injury - consensus statement by the European Drug-Induced Liver Injury Network [PRO-EURO-DILI-NET].

Journal of hepatology

Fernandez-Checa JC, Bagnaninchi P, Ye H, Sancho-Bru P, Falcon-Perez JM, Royo F, Garcia-Ruiz C, Konu O, Miranda J, Lunov O, Dejneka A, Elfick A, McDonald A, Sullivan GJ, Aithal GP, Lucena MI, Andrade RJ, Fromenty B, Kranendonk M, Cubero FJ, Nelson LJ.
PMID: 34171436
J Hepatol. 2021 Oct;75(4):935-959. doi: 10.1016/j.jhep.2021.06.021. Epub 2021 Jun 24.

Drug-induced liver injury (DILI) is a major cause of acute liver failure (ALF) and one of the leading indications for liver transplantation in Western societies. Given the wide use of both prescribed and over the counter drugs, DILI has...

Cite
Fernandez-Checa JC, Bagnaninchi P, Ye H, et al. Advanced preclinical models for evaluation of drug-induced liver injury - consensus statement by the European Drug-Induced Liver Injury Network [PRO-EURO-DILI-NET]. J Hepatol. 2021;75(4):935-959doi: 10.1016/j.jhep.2021.06.021.
Fernandez-Checa, J. C., Bagnaninchi, P., Ye, H., Sancho-Bru, P., Falcon-Perez, J. M., Royo, F., Garcia-Ruiz, C., Konu, O., Miranda, J., Lunov, O., Dejneka, A., Elfick, A., McDonald, A., Sullivan, G. J., Aithal, G. P., Lucena, M. I., Andrade, R. J., Fromenty, B., Kranendonk, M., Cubero, F. J., & Nelson, L. J. (2021). Advanced preclinical models for evaluation of drug-induced liver injury - consensus statement by the European Drug-Induced Liver Injury Network [PRO-EURO-DILI-NET]. Journal of hepatology, 75(4), 935-959. https://doi.org/10.1016/j.jhep.2021.06.021
Fernandez-Checa, Jose C, et al. "Advanced preclinical models for evaluation of drug-induced liver injury - consensus statement by the European Drug-Induced Liver Injury Network [PRO-EURO-DILI-NET]." Journal of hepatology vol. 75,4 (2021): 935-959. doi: https://doi.org/10.1016/j.jhep.2021.06.021
Fernandez-Checa JC, Bagnaninchi P, Ye H, Sancho-Bru P, Falcon-Perez JM, Royo F, Garcia-Ruiz C, Konu O, Miranda J, Lunov O, Dejneka A, Elfick A, McDonald A, Sullivan GJ, Aithal GP, Lucena MI, Andrade RJ, Fromenty B, Kranendonk M, Cubero FJ, Nelson LJ. Advanced preclinical models for evaluation of drug-induced liver injury - consensus statement by the European Drug-Induced Liver Injury Network [PRO-EURO-DILI-NET]. J Hepatol. 2021 Oct;75(4):935-959. doi: 10.1016/j.jhep.2021.06.021. Epub 2021 Jun 24. PMID: 34171436.
Copy Download .nbib Format: NLM
Publisher Correction: The gut-liver axis and the intersection with the microbiome.

Nature reviews. Gastroenterology & hepatology

Tripathi A, Debelius J, Brenner DA, Karin M, Loomba R, Schnabl B, Knight R.
PMID: 29785003
Nat Rev Gastroenterol Hepatol. 2018 Dec;15(12):785. doi: 10.1038/s41575-018-0031-8.

In the original version of Table 1 published online, upward arrows to indicate increased translocation of PAMPs were missing from the row entitled 'Translocation' for both the column on alcoholic liver disease and nonalcoholic fatty liver disease. This error...

Cite
Tripathi A, Debelius J, Brenner DA, et al. Publisher Correction: The gut-liver axis and the intersection with the microbiome. Nat Rev Gastroenterol Hepatol. 2018;15(12):785doi: 10.1038/s41575-018-0031-8.
Tripathi, A., Debelius, J., Brenner, D. A., Karin, M., Loomba, R., Schnabl, B., & Knight, R. (2018). Publisher Correction: The gut-liver axis and the intersection with the microbiome. Nature reviews. Gastroenterology & hepatology, 15(12), 785. https://doi.org/10.1038/s41575-018-0031-8
Tripathi, Anupriya, et al. "Publisher Correction: The gut-liver axis and the intersection with the microbiome." Nature reviews. Gastroenterology & hepatology vol. 15,12 (2018): 785. doi: https://doi.org/10.1038/s41575-018-0031-8
Tripathi A, Debelius J, Brenner DA, Karin M, Loomba R, Schnabl B, Knight R. Publisher Correction: The gut-liver axis and the intersection with the microbiome. Nat Rev Gastroenterol Hepatol. 2018 Dec;15(12):785. doi: 10.1038/s41575-018-0031-8. PMID: 29785003; PMCID: PMC7133393.
Copy Download .nbib Format: NLM
Lysosomal and Mitochondrial Liaisons in Niemann-Pick Disease.

Frontiers in physiology

Torres S, Balboa E, Zanlungo S, Enrich C, Garcia-Ruiz C, Fernandez-Checa JC.
PMID: 29249985
Front Physiol. 2017 Nov 30;8:982. doi: 10.3389/fphys.2017.00982. eCollection 2017.

Lysosomal storage disorders (LSD) are characterized by the accumulation of diverse lipid species in lysosomes. Niemann-Pick type A/B (NPA/B) and type C diseases Niemann-Pick type C (NPC) are progressive LSD caused by loss of function of distinct lysosomal-residing proteins,...

Cite
Torres S, Balboa E, Zanlungo S, et al. Lysosomal and Mitochondrial Liaisons in Niemann-Pick Disease. Front Physiol. 2017;8:982doi: 10.3389/fphys.2017.00982.
Torres, S., Balboa, E., Zanlungo, S., Enrich, C., Garcia-Ruiz, C., & Fernandez-Checa, J. C. (2017). Lysosomal and Mitochondrial Liaisons in Niemann-Pick Disease. Frontiers in physiology, 8982. https://doi.org/10.3389/fphys.2017.00982
Torres, Sandra, et al. "Lysosomal and Mitochondrial Liaisons in Niemann-Pick Disease." Frontiers in physiology vol. 8 (2017): 982. doi: https://doi.org/10.3389/fphys.2017.00982
Torres S, Balboa E, Zanlungo S, Enrich C, Garcia-Ruiz C, Fernandez-Checa JC. Lysosomal and Mitochondrial Liaisons in Niemann-Pick Disease. Front Physiol. 2017 Nov 30;8:982. doi: 10.3389/fphys.2017.00982. eCollection 2017. PMID: 29249985; PMCID: PMC5714892.
Copy Download .nbib Format: NLM
Showing 1 to 12 of 62 entries