Evidence map›Paper›PMID 36349141›Full record

ArticlePrecision clinical medicine2022

Dissection of cellular and molecular mechanisms of aristolochic acid-induced hepatotoxicity via single-cell transcriptomics.

Piao Luo, Jiayun Chen, Qian Zhang, Fei Xia, Chen Wang, Yunmeng Bai, Huan Tang, Dandan Liu, Liwei Gu, Qingfeng Du and 3 more

Open access · diamondAbstract read
In one paragraph

Article in Precision clinical medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

11 citing papers in PubMed, 32 citations in OpenAlex.

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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

13 authors at 4 institutions in 1 country.

Piao LuoDepartment of Geriatric Medicine, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Shenzhen 518020, China.
Jiayun ChenArtemisinin Research Center, and Institute of Chinese Materia Medica, Chinese Academy of Chinese Medical Sciences, Beijing 100700, China.
Qian ZhangDepartment of Geriatric Medicine, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Shenzhen 518020, China.
Fei XiaArtemisinin Research Center, and Institute of Chinese Materia Medica, Chinese Academy of Chinese Medical Sciences, Beijing 100700, China.
Chen WangArtemisinin Research Center, and Institute of Chinese Materia Medica, Chinese Academy of Chinese Medical Sciences, Beijing 100700, China.
Yunmeng BaiDepartment of Geriatric Medicine, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Shenzhen 518020, China.
Huan TangArtemisinin Research Center, and Institute of Chinese Materia Medica, Chinese Academy of Chinese Medical Sciences, Beijing 100700, China.
Dandan LiuArtemisinin Research Center, and Institute of Chinese Materia Medica, Chinese Academy of Chinese Medical Sciences, Beijing 100700, China.
Liwei GuArtemisinin Research Center, and Institute of Chinese Materia Medica, Chinese Academy of Chinese Medical Sciences, Beijing 100700, China.
Qingfeng DuSchool of Traditional Chinese Medicine, Southern Medical University, Guangzhou 510515, China.
Wei XiaoKey Laboratory of Glucolipid Metabolic Disorder, Ministry of Education, Guangdong Pharmaceutical University, Guangzhou 510006, China.
Chuanbin YangDepartment of Geriatric Medicine, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Shenzhen 518020, China.ORCID https://orcid.org/0000-0001-8288-4038
Jigang WangDepartment of Geriatric Medicine, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Shenzhen 518020, China.ORCID https://orcid.org/0000-0002-0575-0105
Chinese Academy of Medical Sciences & Peking Union Medical College · CNJinan University · CNGuangdong Pharmaceutical University · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Aristolochic acids (AAs), a class of carcinogenic and mutagenic natural products from Methods: Here, we aimed to dissect the underlying cellular and molecular mechanisms of aristolochic acid I (AAI)-induced hepatotoxicity by using advanced single-cell RNA sequencing (scRNA-seq) and proteomics techniques. We established the first single-cell atlas of mouse livers in response to AAI. Results: In hepatocytes, our results indicated that AAI activated NF-κB and STAT3 signaling pathways, which may contribute to the inflammatory response and apoptosis. In liver sinusoidal endothelial cells (LSECs), AAI activated multiple oxidative stress and inflammatory associated signaling pathways and induced apoptosis. Importantly, AAI induced infiltration of cytotoxic T cells and activation of proinflammatory macrophage and neutrophil cells in the liver to produce inflammatory cytokines to aggravate inflammation. Conclusions: Collectively, our study provides novel knowledge of AAs-induced molecular characteristics of hepatotoxicity at a single-cell level and suggests future treatment options for AAs associated hepatotoxicity.

Indexed as

aristolochic acidhepatotoxicityproteomicsscRNA-seq

Identifiers

PMID36349141
PMCPMC9635452
OpenAlexW4297006220

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.