Evidence map›Paper›PMID 30131868›Full record

ArticleCell discovery2018

RPS3A positively regulates the mitochondrial function of human periaortic adipose tissue and is associated with coronary artery diseases.

Yan Tang, Yi He, Chen Li, Wenjuan Mu, Ying Zou, Conghui Liu, Shuwen Qian, Fuchuang Zhang, Jiabao Pan, Yina Wang and 6 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell discovery, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 16% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
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  10. Dysregulated fatty acid metabolism in pericardiac adipose tissue of pulmonary hypertension due to left heart disease mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 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

16 authors at 6 institutions in 1 country.

Yan Tang *1Key Laboratory of Metabolism and Molecular Medicine of Chinese Ministry of Education, Department of Biochemistry and Molecular Biology of School of Basic Medical Sciences and Department of Endocrinology of Zhongshan Hospital, Fudan University, 200032 Shanghai, China.
Yi He *2Department of Cardiothoracic Surgery, Xinhua Hospital, Shanghai Jiaotong University of Medicine College, 200032 Shanghai, China.
Chen Li *3Key Laboratory of Systems Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Wenjuan Mu1Key Laboratory of Metabolism and Molecular Medicine of Chinese Ministry of Education, Department of Biochemistry and Molecular Biology of School of Basic Medical Sciences and Department of Endocrinology of Zhongshan Hospital, Fudan University, 200032 Shanghai, China.
Ying Zou1Key Laboratory of Metabolism and Molecular Medicine of Chinese Ministry of Education, Department of Biochemistry and Molecular Biology of School of Basic Medical Sciences and Department of Endocrinology of Zhongshan Hospital, Fudan University, 200032 Shanghai, China.
Conghui Liu3Key Laboratory of Systems Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Shuwen Qian1Key Laboratory of Metabolism and Molecular Medicine of Chinese Ministry of Education, Department of Biochemistry and Molecular Biology of School of Basic Medical Sciences and Department of Endocrinology of Zhongshan Hospital, Fudan University, 200032 Shanghai, China.
Fuchuang Zhang1Key Laboratory of Metabolism and Molecular Medicine of Chinese Ministry of Education, Department of Biochemistry and Molecular Biology of School of Basic Medical Sciences and Department of Endocrinology of Zhongshan Hospital, Fudan University, 200032 Shanghai, China.
Jiabao Pan1Key Laboratory of Metabolism and Molecular Medicine of Chinese Ministry of Education, Department of Biochemistry and Molecular Biology of School of Basic Medical Sciences and Department of Endocrinology of Zhongshan Hospital, Fudan University, 200032 Shanghai, China.
Yina Wang1Key Laboratory of Metabolism and Molecular Medicine of Chinese Ministry of Education, Department of Biochemistry and Molecular Biology of School of Basic Medical Sciences and Department of Endocrinology of Zhongshan Hospital, Fudan University, 200032 Shanghai, China.
Haiyan Huang1Key Laboratory of Metabolism and Molecular Medicine of Chinese Ministry of Education, Department of Biochemistry and Molecular Biology of School of Basic Medical Sciences and Department of Endocrinology of Zhongshan Hospital, Fudan University, 200032 Shanghai, China.
Dongning Pan1Key Laboratory of Metabolism and Molecular Medicine of Chinese Ministry of Education, Department of Biochemistry and Molecular Biology of School of Basic Medical Sciences and Department of Endocrinology of Zhongshan Hospital, Fudan University, 200032 Shanghai, China.
Pengyuan Yang1Key Laboratory of Metabolism and Molecular Medicine of Chinese Ministry of Education, Department of Biochemistry and Molecular Biology of School of Basic Medical Sciences and Department of Endocrinology of Zhongshan Hospital, Fudan University, 200032 Shanghai, China.
Ju Mei2Department of Cardiothoracic Surgery, Xinhua Hospital, Shanghai Jiaotong University of Medicine College, 200032 Shanghai, China.
Rong Zeng3Key Laboratory of Systems Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Qi-Qun Tang1Key Laboratory of Metabolism and Molecular Medicine of Chinese Ministry of Education, Department of Biochemistry and Molecular Biology of School of Basic Medical Sciences and Department of Endocrinology of Zhongshan Hospital, Fudan University, 200032 Shanghai, China.
Fudan University · CNZhongshan Hospital · CNXinHua Hospital · CNCenter for Excellence in Molecular Cell Science · CNChinese Academy of Sciences · CNShanghai Institutes for Biological Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pericardial adipose tissue, which comprises both epicardial adipose tissue (EAT) and paracardial adipose tissue (PAT), has recently been recognized as a novel factor in the pathophysiology of cardiovascular diseases, especially coronary artery disease (CAD). The goal of this study was to evaluate differences in the brown-like characteristic and proteome among human EAT, PAT, and subcutaneous adipose tissue (SAT) to identify candidate molecules causing CAD. Uncoupling protein 1 (UCP-1) and other brown-related proteins were highly expressed in pericardial adipose tissue but was weakly expressed in SAT from the same non-CAD patient. Moreover, pericardial adipose tissues displayed a higher thermogenesis than SAT. However, brown-related genes were lower in CAD pericardial fat. Remarkably, there were lower levels of metabolic enzymes involved in glycolysis, tricarboxylic acid cycle, and fatty acid metabolism in pericardial adipose tissues of CAD. EAT is an organ adjacent to aortic root without anatomy barriers, which differs from PAT. We found that the expression of ribosomal protein S3A (RPS3A) was decreased in human EAT as well as in mouse perivascular adipose tissue (PVAT). Knockdown of RPS3A significantly inhibited adipocyte differentiation in preadipocytes and impaired the function of mitochondria in mature adipocytes. Moreover, RPS3A knockdown in mouse periaortic adipose tissue impaired browning of PVAT, accelerated vascular inflammation, and atherosclerosis progression. Mechanistically, RPS3A can migrate to the mitochondria to maintain the function of brown adipocytes. These findings provide compelling evidence that RPS3A was a key factor for modulating the brown fat-specific gene UCP-1 and carbon metabolic enzymes in EAT for preventing CAD.

Identifiers

PMID30131868
PMCPMC6102269
OpenAlexW2886894136

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Registered trials

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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.