Evidence map›Paper›PMID 38809648›Full record

ArticleAsian Pacific journal of cancer prevention : APJCP2024

Does Autophagy have a Role in the Pathogenesis of Pediatric Hepatic Steatosis?

Marwa Salah Gadallah, Mona Kandil, Nanis Shawky Holah, Gihan Ahmed Sobhy, Mohamed Mohamdy Ahmed, Shymaa Sabry El-Gammal, Nermine Ahmed Ehsan

Abstract read
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Article in Asian Pacific journal of cancer prevention : APJCP, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Marwa Salah GadallahPathology Department, Faculty of Medicine, Menoufia University, Shebin El-Kom, Egypt.
Mona KandilPathology Department, Faculty of Medicine, Menoufia University, Shebin El-Kom, Egypt.
Nanis Shawky HolahPathology Department, Faculty of Medicine, Menoufia University, Shebin El-Kom, Egypt.
Gihan Ahmed SobhyPediatric Department, National Liver Institute, Menoufia University, Shebin El-Kom, Egypt.
Mohamed Mohamdy AhmedBiology Fellow, Pathology Department, Menofia University, Shebin El-Kom, Egypt.
Shymaa Sabry El-GammalNational Liver Institute, Menoufia University, Shebin El-Kom, Egypt.
Nermine Ahmed EhsanDepartment of Pathology, National Liver Institute, Menoufia University, Egypt.ORCID 0000-0003-4493-6647

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatic steatosis has become the most common cause of chronic liver disease among children worldwide.  Lipophagy has been considered as a pathway affecting steatosis development and progression.

objectivethis study aimed to evaluate the immunohistochemical expression of Beclin1 and LC3A in pediatric hepatic tissues with steatosis and to correlate their expression with clinicopathological parameters.

methodsthis study included 81 Egyptian pediatric patients with hepatic steatosis and 21 pediatric cases without hepatic steatosis. All specimens were stained by Beclin1 and LC3A antibodies. According to final diagnosis obtained from Pediatric Hepatology department, patients were divided into two groups: chronic liver disease (CLD) group that included 45 cases and inborn error of metabolism (IEM) group that included 36 cases.

resultshigher beclin1 expression was significantly correlated with higher stages of fibrosis and distorted liver architecture in CLD group, (P=0.043) for both. The control group showed higher positivity, percentage, as well as the median values of the H score of LC3A expression than did the CLD group or the IEM group (P=0.055, 0.001, and 0.008, respectively). Higher positivity of LC3A was significantly associated with higher stages of fibrosis and distorted liver architecture in the studied IEM group (P=0.021) for both.

conclusionsVarying intensity grades of LC3A and Beclin 1 immunohistochemical expression demonstrate the variation of autophagy at different phases of pediatric hepatic steatosis and varied disease etiology.

Indexed as

AutophagyBeclin-1Fatty LiverMicrotubule-Associated ProteinsAdolescentBiomarkersCase-Control StudiesChildChild, PreschoolEgyptFemaleFollow-Up StudiesHumansInfantLiverLiver CirrhosisBeclin-1BECN1 protein, humanBiomarkersMAP1LC3A protein, humanMicrotubule-Associated ProteinsBeclin 1immunohistochemistryLC3ALipophagyNon-alcoholic steatohepatitis

Identifiers

PMID38809648
PMCPMC11318833

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