Evidence map›Paper›PMID 32945983›Full record

ArticleDigestive diseases and sciences2021

FAM172A Deletion May Enhance Hepatic Steatosis by Promoting ER Stress.

Fan Xiao, Meixin Gao, Junru Yang, Lingling He, Hongshan Wei

Abstract read
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In one paragraph

Article in Digestive diseases and sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 89% of its field
1 · What the graph read from it

What it found

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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.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Fan Xiao *Beijing Key Laboratory of Emerging Infectious Diseases, Institute of Infectious Diseases, Beijing Ditan Hospital, Capital Medical University, Beijing, 100015, China.
Meixin Gao *Department of Gastroenterology, Beijing Ditan Hospital, Capital Medical University, Beijing, 100015, China.
Junru YangDepartment of Gastroenterology, Beijing Ditan Hospital, Capital Medical University, Beijing, 100015, China.
Lingling HeDepartment of Gastroenterology, Beijing Ditan Hospital, Capital Medical University, Beijing, 100015, China.
Hongshan WeiDepartment of Gastroenterology, Beijing Ditan Hospital, Capital Medical University, Beijing, 100015, China. drwei@ccmu.edu.cn.ORCID http://orcid.org/0000-0001-8893-653X
Capital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEndoplasmic reticulum (ER) stress is one of the major causes to the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Our previous study showed that maintains the homeostasis of ER could effectively alleviate NAFLD. In this study, we found that the loss of FAM172A increased ER stress.

aimsThe aims of this study were to explore whether FAM172A could improve NAFLD by inhibiting ER stress.

methodsThe expression levels of FAM172A and ER stress were detected by western blot. The method of immunofluorescence was used to determine FAM172A location. The interacted proteins of FAM172A were identified by immunocoprecipitation. The methods of MTS and caspase-3/7 activity were taken to confirm the effect of FAM172A on cell viability and proliferation. The expression levels of inflammation were detected by qPCR.

resultsWe confirmed that FAM172A might alleviate NAFLD through inhibiting ER stress. Loss of FAM172A increased the expressions of ATF6, peIF2α, but decreased the expression of IRE1α. Then, it was shown that FAM172A located in ER and FAM172A directly interacted with ATF6 and peIF2α and IRE1α. More importantly, the binding of FAM172A and eIF2a in tunicamycin-treated group increased significantly compared with the control group. However, the binding of FAM172A and ATF6 or IRE1α did not change. Next, we found that the lack of FAM172A could produce more apoptosis and inflammation.

conclusionsOur results suggest that FAM172A improve steatosis by alleviating ER stress.

Indexed as

ProteinsAnimalsApoptosisCell LineCell ProliferationCell SurvivalEndoplasmic ReticulumEndoplasmic Reticulum StressGene DeletionGene Expression ProfilingGene Expression RegulationLiverMiceNon-alcoholic Fatty Liver DiseaseUnfolded Protein ResponseFam172a protein, mouseProteinsEndoplasmic reticulum stressFAM172ANonalcoholic fatty liver diseaseSteatosis

Identifiers

PMID32945983
OpenAlexW3087403641

What OpenQuestion holds

Textmetadata
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Registered trials

None linked

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.