Evidence map›Paper›PMID 31571967›Full record

ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2019

NLRP3 inflammasome promotes diabetes-induced endothelial inflammation and atherosclerosis.

Zhaofei Wan, Yan Fan, Xiaojun Liu, Jiahong Xue, Zhenhua Han, Canzhan Zhu, Xinhong Wang

Open access · goldAbstract read
In one paragraph

Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
4.2field-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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 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

7 authors at 2 institutions in 1 country.

Zhaofei WanDepartment of Cardiovascular Medicine, Second Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi, People's Republic of China.
Yan FanDepartment of Cardiovascular Medicine, Gansu Provincial Hospital, Lanzhou, People's Republic of China.
Xiaojun LiuDepartment of Cardiovascular Medicine, Second Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi, People's Republic of China.
Jiahong XueDepartment of Cardiovascular Medicine, Second Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi, People's Republic of China.
Zhenhua HanDepartment of Cardiovascular Medicine, Second Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi, People's Republic of China.
Canzhan ZhuDepartment of Cardiovascular Medicine, Second Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi, People's Republic of China.
Xinhong WangDepartment of Cardiovascular Medicine, Second Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi, People's Republic of China.
Second Affiliated Hospital of Xi'an Jiaotong University · CNGansu Provincial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNLRP3 inflammasome can be activated by high glucose and links inflammation and metabolic disease. This study aimed to investigate the role of NLRP3 inflammasome in hyperglycemia-induced endothelial inflammation and diabetic atherosclerosis.

methodsNLRP3 levels in peripheral blood mononuclear cell (PBMC) and plasma IL-1β level were measured in diabetes patients. The activation of NLPR3 was detected in diabetic ApoE-/- mice and human umbilical vein endothelial cells (HUVECs).

resultsCompared with healthy controls, NLRP3 expression levels in PBMC and plasma IL-1β level were significantly higher in diabetes patients but considerably decreased after lifestyle interventions and medicine. Moreover, carotid atherosclerosis was significantly related to plasma IL-1β level in diabetes patients. In diabetic atherosclerosis mouse model, NLRP3 knockdown suppressed NLRP3 inflammasome activation, inhibited the expression of adhesion molecules ICAM-1 and VCAM-1 in intima, reduced atherosclerosis and stabilized atherosclerotic plaque. In vitro, the expression of NLRP3 inflammasome components and the secretion of IL-1β were augmented by high glucose in HUVECs. Moreover, either high glucose or IL-1β promoted the expression of adhesion molecules, which were suppressed by NLRP3 knockdown or IL-1β receptor antagonist.

conclusionThese findings provide novel insights into pathological mechanisms of diabetic atherosclerosis and have potential therapeutic implications for cardiovascular complications in diabetes.

Indexed as

atherosclerosisdiabetesinflammationNLRP3 inflammasome

Identifiers

PMID31571967
PMCPMC6759984
OpenAlexW2974408969

What OpenQuestion holds

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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.