Paediatric non-alcoholic fatty liver disease: an approach to pathological evaluation

Wang, Chiyun; Pai, Anita K; Putra, Juan

doi:10.1136/jclinpath-2022-208246

Cited by 6 publications

(3 citation statements)

References 116 publications

(179 reference statements)

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“…As a consequence, ROS production was lower, leading to a reduction in the progression of liver fibrosis in Casp8 -/- livers 47 . In agreement, curcumin treatment was shown to be beneficial in preventing the development of NASH in rat models by reducing apoptosis and decreasing the expression of Casp8 48 . TSK is a hepatokine induced in response to both endoplasmic reticulum stress and inflammation in severely obese mice.…”

Section: Discussionmentioning

confidence: 55%

RNAseq analysis reveals transcriptome changes associated with the progression of non-alcoholic liver disease in livers fromEfcab4bknockout mice

Cheng,

Pedicini,

Morales Alcala

et al. 2024

Preprint

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EFCAB4B is an evolutionarily conserved protein that encodes for the Rab GTPase Rab46, and the CRAC channel modulator, CRACR2A. Previous genome wide association studies have demonstrated the association of EFCAB4B variants in the progression of non-alcoholic liver disease (NAFLD). In this study we show that mice with global depletion of Efcab4b-/- have significantly larger livers than their wild-type (WT) counterparts. We performed RNA-sequencing (RNA-seq) analysis with liver tissues to investigate differential global gene expression among Efcab4b-/- and WT mice. Of the 69 differentially expressed genes (DEGs), analyses of biological processes found significant enrichment in liver and bile development, with 6 genes (Pck1, Aacs, Onecut1, E2f8, Xbp1, and Hes1) involved in both processes. Specific consideration of possible roles of DEGs or their products in NAFLD progression to (NASH) and hepatocarcinoma (HCC), demonstrated DEGs in the livers of Efcab4b-/- mice had roles in molecular pathways including lipid metabolism, inflammation, ER stress, and fibrosis. The results in this study provide additional insights into molecular mechanisms responsible for increasing susceptibility of liver injuries associated with EFCAB4B.

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Section: Discussionmentioning

confidence: 55%

RNAseq analysis reveals transcriptome changes associated with the progression of non-alcoholic liver disease in livers fromEfcab4bknockout mice

Cheng,

Pedicini,

Morales Alcala

et al. 2024

Preprint

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show abstract

“…As a consequence, ROS production was lower, leading to a reduction in the progression of liver fibrosis in Casp8 -/livers 42 . In agreement, curcumin treatment was shown to be beneficial in preventing the development of NASH in rat models by reducing apoptosis and decreasing the expression of Casp8 43 . TSK is a hepatokine induced in response to both endoplasmic reticulum stress and inflammation in severely obese mice.…”

Section: Inflammation and Er Stress In Nashmentioning

confidence: 55%

RNA-seq analysis reveals transcriptome changes associated with the progression of non-alcoholic liver disease in livers from Efcab4b knockout mice

Cheng,

Pedicini,

Alcala

et al. 2024

Preprint

View full text Add to dashboard Cite

EFCAB4B is an evolutionarily conserved protein that encodes for the Rab GTPase Rab46, and the CRAC channel modulator, CRACR2A. Previous genome wide association studies have demonstrated the association of EFCAB4B variants in the progression of non-alcoholic liver disease (NAFLD). In this study we show that mice with global depletion of Efcab4b-/-have significantly larger livers than their wild-type (WT) counterparts. We performed RNA-sequencing (RNA-seq) analysis of liver tissues to investigate differential global gene expression among Efcab4b-/-and WT mice. Of the 69 differentially expressed genes (DEGs), analyses of biological processes found significant enrichment in liver and bile development, with 6 genes (Pck1, Aacs, Onecut1, E2f8, Xbp1, and Hes1) involved in both processes. Specific consideration of possible roles of DEGs or their products in NAFLD progression to (NASH) and hepatocarcinoma (HCC), demonstrated DEGs in the livers of Efcab4b-/-mice had roles in molecular pathways including lipid metabolism, inflammation, ER stress and fibrosis. The results in this study provide additional insights into molecular mechanisms responsible for increasing susceptibility of liver injuries associated with EFCAB4B.

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“…Standard procedures for liver biopsy handling and processing have been established in several organizations, and guidelines have been collected. 19 – 24 We will divide the handling and processing into three sections, pre-analytical, analytical, and post-analytical. The pre-analytical handling entails taking the biopsy and transferring the material to the department of laboratory medicine and pathology.…”

Section: Introductionmentioning

confidence: 99%

Liver Biopsy Handling of Metabolic-Associated Fatty Liver Disease (MAFLD): the Children’s Hospital of Eastern Ontario grossing protocol

Sergi,

Kehar,

Jimenez-Rivera

2024

Therapeutic Advances in Endocrinology

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Metabolic-(non-alcoholic) associated fatty liver disease (MAFLD/NAFLD) has increasingly become a worldwide epidemic. It has been suggested that renaming NAFLD to MAFLD is critical in identifying patients with advanced fibrosis and poor cardiovascular outcomes. There are concerns that the progression to non-alcoholic steatohepatitis (NASH) may become a constant drive in the future healthcare of children and adolescents. There is a necessity to tackle the emerging risk factors for NASH-associated hepatocellular carcinoma (HCC). In this narrative review, we present the current protocol of liver biopsy separated between pre-analytical, analytical, and post-analytical handling. Genetic association investigations have identified single nucleotide polymorphisms implicated in the progression of MAFLD-HCC, many of which seem to belong to the lipid metabolism pathways. PNPLA3 rs738409 variant, TM6SF2 rs58542926 variant, MBOAT7 rs641738 variant, and GCKR variants seem to be significantly associated with NAFLD disease susceptibility. In disclosing the current comprehensive protocol performed at the Children’s Hospital of Eastern Ontario, Ottawa, ON, Canada, we support the most recent Kulkarni-Sarin’s pledge to rename NAFLD to MAFLD. Grossing of the liver biopsy is key to identifying histologic, immunophenotypical, and ultrastructure data and properly preserving tissue for molecular genomics data.

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Paediatric non-alcoholic fatty liver disease: an approach to pathological evaluation

Cited by 6 publications

References 116 publications

RNAseq analysis reveals transcriptome changes associated with the progression of non-alcoholic liver disease in livers fromEfcab4bknockout mice

RNAseq analysis reveals transcriptome changes associated with the progression of non-alcoholic liver disease in livers fromEfcab4bknockout mice

RNA-seq analysis reveals transcriptome changes associated with the progression of non-alcoholic liver disease in livers from Efcab4b knockout mice

Liver Biopsy Handling of Metabolic-Associated Fatty Liver Disease (MAFLD): the Children’s Hospital of Eastern Ontario grossing protocol

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