ReviewPancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]2015
Metabolic reprogramming and cell fate regulation in alcoholic liver disease.
Review in Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.], 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Modeling alcohol-associated liver disease in a human Liver-Chip.Cell reports · 2021Article
- A Novel Mouse Model of Acute-on-Chronic Cholestatic Alcoholic Liver Disease: A Systems Biology Comparison With Human Alcoholic Hepatitis.Alcoholism, clinical and experimental research · 2020Article
- Synergistic effects ofAmerican journal of translational research · 2019Article
- Supplements of vitamins B9 and B12 affect hepatic and mammary gland gene expression profiles in lactating dairy cows.BMC genomics · 2016Article
- Regulation of transforming growth factor-beta1 (TGF-β1)-induced pro-fibrotic activities by circadian clock gene BMAL1.Respiratory research · 2016Article
- Hepatocellular Carcinoma, Fibrolamellar Variant: Diagnostic Pathologic Criteria and Molecular Pathology Update. A Primer.Diagnostics (Basel, Switzerland) · 2015Article
- Update on Alcoholic Hepatitis.Biomolecules · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
unlabelledAlcoholic liver disease (ALD) should be defined as a life-style metabolic disease. Its pathogenesis is driven by altered cell fate of both parenchymal and non-parenchymal liver cell types, contributing to different pathologic spectra. A critical turning point in progression of ALD is chronic alcoholic steatohepatitis (ASH) or alcoholic neutrophilic hepatitis (AH), which markedly predisposes patients to most devastating ALD sequela, cirrhosis and liver cancer.
resultsOur research identifies the pivotal roles of unique metabolic reprogramming in M1 activation of hepatic macrophages (HM) and myofibroblastic activation (MF) of hepatic stellate cells (HSC) in the genesis of inflammation and fibrosis, the two key histological features of chronic ASH and neutrophilic AH. For M1 HM activation, heightened proinflammatory iron redox signaling in endosomes or caveosomes results from altered iron metabolism and storage, promoting IKK/NF-kB activation via interactive activation of p21ras, TAK1, and PI3K. For MF cell fate regulation of HSC, activation of the morphogen Wnt pathway caused by the nuclear protein NECDIN or the single-pass trans-membrane protein DLK1, reprograms lipid metabolism via MeCP2-mediated epigenetic repression of the key HSC quiescence gene Ppar-γ.
conclusionsThe findings from these studies re-enforce the importance of metabolic reprogramming in cell fate regulation required for the pathogenesis of ALD.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.