Evidence map›Paper›PMID 33246954›Full record

ArticleScience advances2020

CRISPR-mediated BMP9 ablation promotes liver steatosis via the down-regulation of PPARα expression.

Z Yang, P Li, Q Shang, Y Wang, J He, S Ge, R Jia, X Fan

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 48 citations in OpenAlex.

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  5. Targeting the Liver Serine Protease TMPRSS6 Ameliorates Steatosis and Attenuates Fibrosis in Experimental MASLD.Liver international : official journal of the International Association for the Study of the Liver · 2025
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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 2 institutions in 1 country.

Z YangDepartment of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 833 Zhizaoju Road, Shanghai 200011, China.ORCID 0000-0001-9440-7896
P LiDepartment of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 833 Zhizaoju Road, Shanghai 200011, China.ORCID 0000-0003-3365-0264
Q ShangDepartment of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 833 Zhizaoju Road, Shanghai 200011, China.ORCID 0000-0002-3310-5170
Y WangDepartment of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 833 Zhizaoju Road, Shanghai 200011, China.ORCID 0000-0003-2010-7342
J HeDepartment of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 833 Zhizaoju Road, Shanghai 200011, China.ORCID 0000-0001-7034-1685
S GeDepartment of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 833 Zhizaoju Road, Shanghai 200011, China. geshengfang@sjtu.edu.cn jiarengbing@sjtu.edu.cn fanxq@sjtu.edu.cn.ORCID 0000-0002-8005-2462
R JiaDepartment of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 833 Zhizaoju Road, Shanghai 200011, China. geshengfang@sjtu.edu.cn jiarengbing@sjtu.edu.cn fanxq@sjtu.edu.cn.ORCID 0000-0001-6642-7451
X FanDepartment of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, 833 Zhizaoju Road, Shanghai 200011, China. geshengfang@sjtu.edu.cn jiarengbing@sjtu.edu.cn fanxq@sjtu.edu.cn.ORCID 0000-0002-9394-3969
Shanghai Ninth People's Hospital · CNShanghai Institute of Nutrition and Health · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity drives the development of nonalcoholic fatty liver disease (NAFLD) characterized by hepatic steatosis. Several bone morphogenetic proteins (BMPs) except BMP9 were reported related to metabolic syndrome. This study demonstrates that liver cytokine BMP9 is decreased in the liver and serum of NAFLD model mice and patients. BMP9 knockdown induces lipid accumulation in Hepa 1-6 cells. BMP9-knockout mice exhibit hepatosteatosis due to down-regulated peroxisome proliferator-activated receptor α (PPARα) expression and reduced fatty acid oxidation. In vitro, recombinant BMP9 treatment attenuates triglyceride accumulation by enhancing PPARα promoter activity via the activation of p-smad. PPARα-specific antagonist GW6471 abolishes the effect of BMP9 knockdown. Furthermore, adeno-associated virus-mediated BMP9 overexpression in mouse liver markedly relieves liver steatosis and obesity-related metabolic syndrome. These findings indicate that BMP9 plays a critical role in regulating hepatic lipid metabolism in a PPARα-dependent manner and may provide a previously unknown insight into NAFLD therapeutic approaches.

Indexed as

Growth Differentiation Factor 2Metabolic SyndromeNon-alcoholic Fatty Liver DiseaseAnimalsClustered Regularly Interspaced Short Palindromic RepeatsDown-RegulationHumansLipid MetabolismLiverMiceMice, Inbred C57BLObesityPPAR alphaGDF2 protein, humanGdf2 protein, mouseGrowth Differentiation Factor 2PPAR alpha

Identifiers

PMID33246954
PMCPMC7695473
OpenAlexW3106831132

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.