In one paragraphArticle in Journal of physiology and biochemistry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 40% of its field
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 registryThe 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 literatureWho cites it
0 citing papers in PubMed, 1 citations in OpenAlex.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
12 authors at 3 institutions in 1 country.
Pengfei Wei *Department of Endocrinology and Metabolism, Shenzhen University General Hospital and Shenzhen University Academy of Clinical Medical Sciences, Shenzhen University, Shenzhen, 518052, Guangdong, China.ORCID http://orcid.org/0000-0002-1315-6384 Mingyue JinDepartment of Endocrinology and Metabolism, Shenzhen University General Hospital and Shenzhen University Academy of Clinical Medical Sciences, Shenzhen University, Shenzhen, 518052, Guangdong, China.ORCID http://orcid.org/0000-0003-0552-8608 Huijuan ZhaoDepartment of Endocrinology and Metabolism, Shenzhen University General Hospital and Shenzhen University Academy of Clinical Medical Sciences, Shenzhen University, Shenzhen, 518052, Guangdong, China.ORCID http://orcid.org/0000-0003-1909-8696 Kelaier YangDepartment of Endocrinology and Metabolism, Shenzhen University General Hospital and Shenzhen University Academy of Clinical Medical Sciences, Shenzhen University, Shenzhen, 518052, Guangdong, China.ORCID http://orcid.org/0000-0002-2840-7510 Yu WangDepartment of Endocrinology and Metabolism, Shenzhen University General Hospital and Shenzhen University Academy of Clinical Medical Sciences, Shenzhen University, Shenzhen, 518052, Guangdong, China.ORCID http://orcid.org/0000-0001-7873-4002 Huaqiu HeDepartment of Endocrinology and Metabolism, Shenzhen University General Hospital and Shenzhen University Academy of Clinical Medical Sciences, Shenzhen University, Shenzhen, 518052, Guangdong, China.ORCID http://orcid.org/0000-0003-2246-5362 Mengyang JiaDepartment of Endocrinology and Metabolism, Shenzhen University General Hospital and Shenzhen University Academy of Clinical Medical Sciences, Shenzhen University, Shenzhen, 518052, Guangdong, China.ORCID http://orcid.org/0000-0003-3914-8304 Hongyan PanDepartment of Endocrinology and Metabolism, Shenzhen University General Hospital and Shenzhen University Academy of Clinical Medical Sciences, Shenzhen University, Shenzhen, 518052, Guangdong, China.ORCID http://orcid.org/0000-0002-5724-8731 Qiang LiDepartment of Endocrinology and Metabolism, Shenzhen University General Hospital and Shenzhen University Academy of Clinical Medical Sciences, Shenzhen University, Shenzhen, 518052, Guangdong, China. qiangli@szu.edu.cn.ORCID http://orcid.org/0000-0002-8268-7883 Jing GuoDepartment of Endocrinology and Metabolism, Shenzhen University General Hospital and Shenzhen University Academy of Clinical Medical Sciences, Shenzhen University, Shenzhen, 518052, Guangdong, China. guojing@szu.edu.cn.ORCID http://orcid.org/0000-0002-7165-965X Shenzhen University · CNGuangdong Medical College · CNShenzhen University Health Science Center · CN
Funding
National Natural Science Foundation of China 81900517Shenzhen Science and Technology Innovation Program JCYJ20190808151805516
6 · The paper itselfAbstract
The global prevalence and incidence of non-alcoholic fatty liver disease (NAFLD) are exhibiting an increasing trend. NAFLD is characterized by a significant accumulation of lipids, though its underlying mechanism is still unknown. Here we report that high-fat diet (HFD) feeding induced hepatic steatosis in mice, which was accompanied by a reduction in the expression and function of hepatic TRPV2. Moreover, conditional knockout of TRPV2 in hepatocytes exacerbated HFD-induced hepatic steatosis. In an in vitro model of NAFLD, TRPV2 regulated lipid accumulation in HepG2 cells, and TRPV2 activation inhibited the expression of the cellular senescence markers p21 and p16, all of which were mediated by AMPK phosphorylation. Finally, we found that administration of probenecid, a TRPV2 agonist, impaired HFD-induced hepatic steatosis and suppressed HFD-induced elevation in p21 and p16. Collectively, our findings imply that hepatic TRPV2 protects against the accumulation of lipids by modulating p21 signalling.
Indexed as
Calcium ChannelsDiet, High-FatNon-alcoholic Fatty Liver DiseaseTRPV Cation ChannelsAnimalsCyclin-Dependent Kinase Inhibitor p21Down-RegulationHepatocytesLipid MetabolismLipidsLiverMiceMice, Inbred C57BLCalcium ChannelsCdkn1a protein, mouseCyclin-Dependent Kinase Inhibitor p21LipidsTrpv2 protein, mouseTRPV Cation ChannelsFatty liverHepatic steatosisLipid accumulationp21TRPV2
Identifiers
PMID37882938
OpenAlexW4387949847
What OpenQuestion holds
Textmetadata
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