2023
Nonalcoholic liver disease: Epidemiology, risk factors, natural history, and management strategies
Agyapong G, Dashti F, Banini B. Nonalcoholic liver disease: Epidemiology, risk factors, natural history, and management strategies. Annals Of The New York Academy Of Sciences 2023, 1526: 16-29. PMID: 37400359, PMCID: PMC10524684, DOI: 10.1111/nyas.15012.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsMeSH KeywordsDisease ProgressionFibrosisHumansLiverLiver CirrhosisNon-alcoholic Fatty Liver DiseaseRisk FactorsUnited StatesConceptsNonalcoholic fatty liver diseaseNonalcoholic fatty liverLiver diseaseRisk factorsCommon chronic liver diseaseEnd-stage liver diseaseNatural historyNAFLD risk factorsChronic liver diseaseFatty liver diseaseCurrent management strategiesClinicopathologic spectrumLiver transplantationNonalcoholic steatohepatitisProgressive fibrosisFatty liverHepatocellular cancerLeading indicationDiseaseUnited StatesManagement strategiesCirrhosisSteatohepatitisTransplantationFibrosis
2022
The Independent Effect of Exercise on Biopsy-Proven Non-Alcoholic Fatty Liver Disease: A Systematic Review
Chen G, Banini B, Do A, Lim J. The Independent Effect of Exercise on Biopsy-Proven Non-Alcoholic Fatty Liver Disease: A Systematic Review. Clinical And Molecular Hepatology 2022, 29: s319-s332. PMID: 36517000, PMCID: PMC10029942, DOI: 10.3350/cmh.2022.0366.Peer-Reviewed Original ResearchMeSH KeywordsBiomarkersBiopsyHumansLiverLiver CirrhosisMagnetic Resonance ImagingNon-alcoholic Fatty Liver DiseaseConceptsNon-alcoholic fatty liver diseaseBiopsy-proven non-alcoholic fatty liver diseaseNon-invasive testsFatty liver diseaseHepatic steatosisLiver fibrosisLiver diseaseHistological endpointsIndependent effectsSystematic reviewNon-randomized interventional studyMagnetic resonance imaging-based techniquesAdditional large RCTsChronic liver diseaseSignificant histological improvementEffects of exerciseClinical outcome endpointsSystematic literature searchHistological improvementExercise interventionHepatocyte ballooningOriginal research studiesLarge RCTsOutcome endpointsInterventional studyHepatic Hydrothorax: An Independent Predictor of Mortality in Cirrhosis? Is the MELD-Na Score Worth Its Salt?
Asotibe JC, Banini BA. Hepatic Hydrothorax: An Independent Predictor of Mortality in Cirrhosis? Is the MELD-Na Score Worth Its Salt? Digestive Diseases And Sciences 2022, 67: 4609-4611. PMID: 35534743, DOI: 10.1007/s10620-022-07523-7.Commentaries, Editorials and LettersMeSH KeywordsHumansHydrothoraxLiver CirrhosisPrognosisRetrospective StudiesSeverity of Illness IndexSodiumDerivation and Validation of a Model to Predict Clinically Significant Portal Hypertension Using Transient Elastography and FIB-4
Banini BA, Patel S, Yu JW, Kang L, Bailey C, Strife BJ, Siddiqui MS, Patel V, Matherly SC, Lee H, Lewis S, Cherian R, Stravitz RT, Luketic V, Sanyal AJ, Sterling RK. Derivation and Validation of a Model to Predict Clinically Significant Portal Hypertension Using Transient Elastography and FIB-4. Journal Of Clinical Gastroenterology 2022, 57: 189-197. PMID: 34999644, PMCID: PMC9271129, DOI: 10.1097/mcg.0000000000001664.Peer-Reviewed Original ResearchMeSH KeywordsElasticity Imaging TechniquesHumansHypertension, PortalLiverLiver CirrhosisRetrospective StudiesConceptsHepatic venous pressure gradientSignificant portal hypertensionFIB-4Chronic liver diseaseAdvanced fibrosisPortal hypertensionLiver biopsyLiver diseasePlatelet countPositive predictive value 27Negative predictive value 99Venous pressure gradientTransjugular liver biopsyGold standardInternal bootstrap validationExternal validationLiver histologyFibrosis indexCurrent gold standardTransient elastographyOptimal cutoffBootstrap validationPatientsSpecificity 67Value 99
2021
Identification of a Metabolic, Transcriptomic, and Molecular Signature of Patatin‐Like Phospholipase Domain Containing 3–Mediated Acceleration of Steatohepatitis
Banini BA, Kumar DP, Cazanave S, Seneshaw M, Mirshahi F, Santhekadur PK, Wang L, Guan HP, Oseini AM, Alonso C, Bedossa P, Koduru SV, Min H, Sanyal AJ. Identification of a Metabolic, Transcriptomic, and Molecular Signature of Patatin‐Like Phospholipase Domain Containing 3–Mediated Acceleration of Steatohepatitis. Hepatology 2021, 73: 1290-1306. PMID: 33131062, PMCID: PMC8046714, DOI: 10.1002/hep.31609.Peer-Reviewed Original Research
2020
Multidisciplinary Management of Hepatic Hydrothorax in 2020: An Evidence‐Based Review and Guidance
Banini BA, Alwatari Y, Stovall M, Ogden N, Gershman E, Shah RD, Strife BJ, Shojaee S, Sterling RK. Multidisciplinary Management of Hepatic Hydrothorax in 2020: An Evidence‐Based Review and Guidance. Hepatology 2020, 72: 1851-1863. PMID: 32585037, DOI: 10.1002/hep.31434.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsKnockout of sulfatase 2 is associated with decreased steatohepatitis and fibrosis in a mouse model of nonalcoholic fatty liver disease
Kim TH, Banini BA, Asumda FZ, Campbell NA, Hu C, Moser CD, Shire AM, Han S, Ma C, Krishnan A, Mounajjed T, White TA, Gores GJ, LeBrasseur NK, Charlton MR, Roberts LR. Knockout of sulfatase 2 is associated with decreased steatohepatitis and fibrosis in a mouse model of nonalcoholic fatty liver disease. AJP Gastrointestinal And Liver Physiology 2020, 319: g333-g344. PMID: 32683952, PMCID: PMC7509257, DOI: 10.1152/ajpgi.00150.2019.Peer-Reviewed Original ResearchConceptsFast food dietStandard chow dietWT miceDiet-induced steatohepatitisNonalcoholic steatohepatitisSulfatase 2Hepatic fibrosisMouse modelStandard chow diet ad libitumChow diet ad libitumNonalcoholic fatty liver diseaseDiet-induced mouse modelConditions of overnutritionProtein expressionFatty liver diseasePotential therapeutic mechanismWild-type miceDiet ad libitumThreefold increaseLiver diseaseChow dietKO miceLiver fibrosisSteatohepatitisMurine model
2017
The Transcriptomic Signature Of Disease Development And Progression Of Nonalcoholic Fatty Liver Disease
Cazanave S, Podtelezhnikov A, Jensen K, Seneshaw M, Kumar DP, Min HK, Santhekadur PK, Banini B, Mauro AG, M. Oseini A, Vincent R, Tanis KQ, Webber AL, Wang L, Bedossa P, Mirshahi F, Sanyal AJ. The Transcriptomic Signature Of Disease Development And Progression Of Nonalcoholic Fatty Liver Disease. Scientific Reports 2017, 7: 17193. PMID: 29222421, PMCID: PMC5722878, DOI: 10.1038/s41598-017-17370-6.Peer-Reviewed Original ResearchConceptsNonalcoholic fatty liver diseaseFatty liver diseaseAdvanced fibrosisLiver diseaseMacrophage activationPathway activationHepatic stellate cell activationFatty liver developmentStellate cell activationOxidative stress pathwaysCell deathAdvanced diseaseMetabolic pathway activationChow dietFatty liverEarly fibrosisFibrogenic pathwaysCell stressSuch miceAnimal modelsCell activationFibrosisMetabolic perturbationsDiseaseOxidative stressCurrent and future pharmacologic treatment of nonalcoholic steatohepatitis
Banini BA, Sanyal AJ. Current and future pharmacologic treatment of nonalcoholic steatohepatitis. Current Opinion In Gastroenterology 2017, 33: 134-141. PMID: 28346237, PMCID: PMC5491795, DOI: 10.1097/mog.0000000000000356.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsNonalcoholic fatty liver diseaseEnd-stage liver diseaseNonalcoholic steatohepatitisLiver diseaseTrend of NAFLDChemokine receptor type 2Future pharmacologic treatmentsCornerstone of therapyStage liver diseaseFatty liver diseasePeroxisome proliferator activator receptorProgression of fibrosisAnti-inflammatory agentsDietary caloric restrictionGlucagon-like peptide 1 pathwayReceptor type 2Liver histologyMetabolic endotoxemiaPharmacologic treatmentTherapeutic optionsHepatocellular cancerAntifibrotic agentsIntestinal microbiomeAggressive formPharmacologic target
2014
Brivanib Attenuates Hepatic Fibrosis In Vivo and Stellate Cell Activation In Vitro by Inhibition of FGF, VEGF and PDGF Signaling
Nakamura I, Zakharia K, Banini BA, Mikhail DS, Kim TH, Yang JD, Moser CD, Shaleh HM, Thornburgh SR, Walters I, Roberts LR. Brivanib Attenuates Hepatic Fibrosis In Vivo and Stellate Cell Activation In Vitro by Inhibition of FGF, VEGF and PDGF Signaling. PLOS ONE 2014, 9: e92273. PMID: 24710173, PMCID: PMC3977817, DOI: 10.1371/journal.pone.0092273.Peer-Reviewed Original ResearchMeSH KeywordsAlanineAnimalsCarbon Tetrachloride PoisoningCell LineCell ProliferationCell SurvivalCollagen Type ICollagen Type I, alpha 1 ChainFibroblast Growth FactorsHepatic Stellate CellsHumansImmunohistochemistryLiver CirrhosisLiver NeoplasmsMicePlatelet-Derived Growth FactorProtein Kinase InhibitorsSignal TransductionTriazinesVascular Endothelial Growth Factor AConceptsVascular endothelial growth factor receptorHuman hepatic stellate cellsBile duct ligationLiver fibrosisStellate cell activationPlatelet-derived growth factorCell activationHuman hepatic stellate cell activationChronic thioacetamide administrationHepatic stellate cell activationInhibition of VEGFREndothelial growth factor receptorChronic carbon tetrachlorideNovel therapeutic approachesHepatic stellate cellsStellate cell proliferationSmooth muscle actinDifferent animal modelsLX-2 human hepatic stellate cellsGrowth factor receptorHepatic fibrosisBrivanibDuct ligationLiver cancerTherapeutic approaches