Evidence map›Paper›PMID 39592735›Full record

ArticleActa pharmacologica Sinica2025

Acid-sensing ion channel 1a promotes alcohol-associated liver disease in mice via regulating endoplasmic reticulum autophagy.

Yue-Qin Zhu, Li-Li Wang, Zi-Hao Li, Shi-Shun Qian, Zhou Xu, Jin Zhang, Yong-Hu Song, Xue-Sheng Pan, Na Du, Amira Abou-Elnour and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta pharmacologica Sinica, 2025. 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
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
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

15 authors.

Yue-Qin Zhu *Department of Pharmacy, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230001, China.
Li-Li Wang *Anhui Province Key Laboratory of Major Autoimmune Diseases, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei, 230032, China.
Zi-Hao Li *Anhui Province Key Laboratory of Major Autoimmune Diseases, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei, 230032, China.
Shi-Shun QianAnhui Province Key Laboratory of Major Autoimmune Diseases, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei, 230032, China.
Zhou XuAnhui Province Key Laboratory of Major Autoimmune Diseases, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei, 230032, China.
Jin ZhangThe First Affiliated Hospital of Anhui Medical University, Hefei, 230032, China.
Yong-Hu SongThe First Affiliated Hospital of Anhui Medical University, Hefei, 230032, China.
Xue-Sheng PanDepartment of Immunology, School of Basic Medical Sciences, Anhui Medical University, Hefei, 230032, China.
Na DuDepartment of Pharmacy, Shanghai Songjiang District Central Hospital, Shanghai, 201600, China.
Amira Abou-ElnourAnhui Province Key Laboratory of Major Autoimmune Diseases, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei, 230032, China.
Lynn Jia TayAnhui Province Key Laboratory of Major Autoimmune Diseases, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei, 230032, China.
Jing-Rong ZhangAnhui Province Key Laboratory of Major Autoimmune Diseases, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei, 230032, China.
Meng-Xue LiAnhui Province Key Laboratory of Major Autoimmune Diseases, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei, 230032, China.
Yu-Xian ShenDepartment of Pharmacology, School of Basic Medical Sciences, Anhui Medical University, Hefei, 230032, China. shenyx@ahmu.edu.cn.
Yan HuangAnhui Province Key Laboratory of Major Autoimmune Diseases, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei, 230032, China. huangyan_@ahmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alcohol-associated liver disease (ALD) is a hepatocyte dysfunction disease caused by chronic or excessive alcohol consumption, which can lead to extensive hepatocyte necrosis and even liver failure. Currently, the pathogenesis of ALD and the anti-ALD mechanisms have not been fully elucidated yet. In this study, we investigated the effects of endoplasmic reticulum autophagy (ER-phagy) in ALD and the role of acid-sensing ion channel 1a (ASIC1a) in ER stress-mediated ER-phagy. A mouse model of ALD was established using the Gao-Binge method and the AML12 cell line treated with alcohol was used as an in vitro model. We showed that ASIC1a expression was significantly increased and ER-phagy was activated in both the in vivo and in vitro models. In alcohol-treated AML12 cells, we showed that blockade of ASIC1a with PcTx-1 or knockdown of ASIC1a reduced alcohol-induced intracellular Ca

Indexed as

Acid Sensing Ion ChannelsAutophagyEndoplasmic ReticulumEndoplasmic Reticulum StressEthanolLiver Diseases, AlcoholicMice, Inbred C57BLAnimalsApoptosisCalciumCell LineHepatocytesMaleMicePeptidesSpider VenomsAcid Sensing Ion ChannelsASIC1 protein, mouseCalciumEthanolPcTX1 protein, Psalmopoeus cambridgeiPeptidesSpider Venomsalcohol-associated liver diseaseapoptosisASIC1aCa2+ influxER-phagyER stress

Identifiers

PMID39592735
PMCPMC11950321

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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.