Evidence map›Paper›PMID 32323149›Full record

ArticleTranslational stroke research2020

Low Serum Uric Acid Levels Promote Hypertensive Intracerebral Hemorrhage by Disrupting the Smooth Muscle Cell-Elastin Contractile Unit and Upregulating the Erk1/2-MMP Axis.

Ning Xiao, Tian-Long Liu, Hao Li, Hao-Chen Xu, Jing Ge, Hong-Yan Wen, Cong-Xia Bai, Li Song, Ying-Ying Sun, Yin-Hui Zhang and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Translational stroke research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
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  4. Lower time-averaged serum uric acid was associated with increased mortality in peritoneal dialysis patients.Therapeutic apheresis and dialysis : official peer-reviewed journal of the International Society for Apheresis, the Japanese Society for Apheresis, the Japanese Society for Dialysis Therapy · 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

13 authors at 1 institution in 1 country.

Ning XiaoState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, 100037, China.
Tian-Long LiuState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, 100037, China.
Hao LiState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, 100037, China.
Hao-Chen XuState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, 100037, China.
Jing GeState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, 100037, China.
Hong-Yan WenState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, 100037, China.
Cong-Xia BaiState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, 100037, China.
Li SongState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, 100037, China.
Ying-Ying SunState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, 100037, China.
Yin-Hui ZhangState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, 100037, China.
Ru-Tai HuiState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, 100037, China.
Wei-Hua SongState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, 100037, China. songweihua926@163.com.
Jing-Zhou ChenState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, 100037, China. chendragon1976@aliyun.com.ORCID http://orcid.org/0000-0002-1642-003X
Chinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

CAMS Innovation Fund for Medical Sciences CAMS-I2M, 2016-I2M-1-015National Basic Research Program of China (973 Program) 2014CB541600 to JCNational Natural Science Foundation of China 81670386National Natural Science Foundation of China 91539113
6 · The paper itself

Abstract

Intracerebral hemorrhage (ICH) is a catastrophic stroke with high mortality, and the mechanism underlying ICH is largely unknown. Previous studies have shown that high serum uric acid (SUA) levels are an independent risk factor for hypertension, cardiovascular disease (CVD), and ischemic stroke. However, our metabolomics data showed that SUA levels were lower in recurrent intracerebral hemorrhage (R-ICH) patients than in ICH patients, indicating that lower SUA might contribute to ICH. In this study, we confirmed the association between low SUA levels and the risk for recurrence of ICH and for cardiac-cerebral vascular mortality in hypertensive patients. To determine the mechanism by which low SUA effects ICH pathogenesis, we developed the first low SUA mouse model and conducted transcriptome profiling of the cerebrovasculature of ICH mice. When combining these assessments with pathological morphology, we found that low SUA levels led to ICH in mice with angiotensin II (Ang II)-induced hypertension and aggravated the pathological progression of ICH. In vitro, our results showed that p-Erk1/2-MMP axis were involved in the low UA-induce degradation of elastin, and that physiological concentrations of UA and p-Erk1/2-specific inhibitor exerted a protective role. This is the first report describing to the disruption of the smooth muscle cell (SMC)-elastin contractile units in ICH. Most importantly, we revealed that the upregulation of the p-Erk1/2-MMP axis, which promotes the degradation of elastin, plays a vital role in mediating low SUA levels to exacerbate cerebrovascular rupture during the ICH process.

Indexed as

AnimalsCerebral HemorrhageHumansHypertensionIntracranial Hemorrhage, HypertensiveMAP Kinase Signaling SystemMatrix MetalloproteinasesMiceMyocytes, Smooth MuscleRisk FactorsStrokeUp-RegulationUric AcidMatrix MetalloproteinasesUric AcidErk1/2Intracerebral hemorrhageMMPsUric acid

Identifiers

PMID32323149
OpenAlexW3018606637

What OpenQuestion holds

Textmetadata
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.