Evidence map›Paper›PMID 37931656›Full record

ArticleJournal of advanced research2024

ASIC1/RIP1 accelerates atherosclerosis via disrupting lipophagy.

Yuan-Mei Wang, Huang Tang, Ya-Jie Tang, Juan Liu, Yu-Fang Yin, Ya-Ling Tang, Yao-Guang Feng, Hong-Feng Gu

Open access · goldAbstract read
In one paragraph

Article in Journal of advanced research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 11% of its field
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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

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  4. Nanomaterials-Based Immunotherapy for Atherosclerosis.Small (Weinheim an der Bergstrasse, Germany) · 2026
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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

8 authors at 6 institutions in 2 countries.

Yuan-Mei WangDepartment of Physiology & Institute of Neuroscience, Hengyang Medical College, University of South China, Hengyang 421001, Hunan, People's Republic of China; College of Life Sciences, University of Chinese Academy of Sciences, Beijing 100049, People's Republic of China.
Huang TangLhasa Guangsheng Hospital, 850000 Tibet, People's Republic of China.
Ya-Jie TangDepartment of Cardiovascular Surgery, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, People's Republic of China.
Juan LiuDepartment of Physiology & Institute of Neuroscience, Hengyang Medical College, University of South China, Hengyang 421001, Hunan, People's Republic of China.
Yu-Fang YinDepartment of Neuroscience and Pharmacology, School of Medicine, Southern Illinois University Springfield, Illinois, United States.
Ya-Ling TangDepartment of Physiology & Institute of Neuroscience, Hengyang Medical College, University of South China, Hengyang 421001, Hunan, People's Republic of China. Electronic address: tangyaling7508@163.com.
Yao-Guang FengDepartment of Cardiothoracic Surgery, The First Affiliated Hospital of University of South China, Hengyang 421001, Hunan, People's Republic of China. Electronic address: fengyaog@hotmail.com.
Hong-Feng GuDepartment of Physiology & Institute of Neuroscience, Hengyang Medical College, University of South China, Hengyang 421001, Hunan, People's Republic of China. Electronic address: ghf513@usc.edu.cn.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNSouthern Illinois University School of Medicine · USFirst Affiliated Hospital of University of South China · CNTibet Autonomous Region People's Hospital · CNUniversity of Chinese Academy of Sciences · CNUniversity of South China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAtherosclerosis, a major contributor to cardiovascular disease, remains a significant health concern worldwide. While previous research has shown that acid-sensing ion channel 1 (ASIC1) impedes macrophage cholesterol efflux, its precise role in atherogenesis and the underlying mechanisms have remained elusive.

objectivesThis study aimed to investigate the role of ASIC1 in atherosclerosis and its underlying mechanisms.

methodsFirst, data from a single-cell RNA sequencing (scRNA-seq) database were used to explore the relationships between ASIC1 differential expression and lipophagy in human atherosclerotic lesions. Finally, we validated the role of ASIC1/RIP1 signaling in lipophagy in vivo (human and mice) and in vitro (RAW264.7 and HTP-1 cells).

resultOur results demonstrated a significant increase in ASIC1 protein levels within CD68+ macrophages in both human aortic lesions and AopE

conclusionOur findings unveil the critical role of macrophage ASIC1 in interacting with RIP1 to inhibit lipophagy, thereby promoting atherogenesis. Targeting ASIC1 represents a promising therapeutic avenue for the treatment of atherosclerosis.

Indexed as

Acid Sensing Ion ChannelsAtherosclerosisMacrophagesAnimalsAutophagyGTPase-Activating ProteinsHumansLipid MetabolismMaleMiceMice, Inbred C57BLMice, KnockoutPhosphorylationRAW 264.7 CellsReceptor-Interacting Protein Serine-Threonine KinasesSignal TransductionAcid Sensing Ion ChannelsASIC1 protein, humanASIC1 protein, mouseGTPase-Activating ProteinsReceptor-Interacting Protein Serine-Threonine KinasesRIPK1 protein, humanRipk1 protein, mouseASIC1AtherosclerosisLipid accumulationLipophagyRIP1

Identifiers

PMID37931656
PMCPMC11379975
OpenAlexW4388336361

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.