Evidence map›Paper›PMID 29643819›Full record

ArticleFrontiers in physiology2018

HMGB1 Increases IL-1β Production in Vascular Smooth Muscle Cells via NLRP3 Inflammasome.

Eun Jung Kim, So Youn Park, Seung Eun Baek, Min A Jang, Won Suk Lee, Sun Sik Bae, Koanhoi Kim, Chi Dae Kim

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
7.9field-weighted citation impact, top 2% 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

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.

  1. Pooled it
  2. HMGB1 as a danger signal in vascular remodeling.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
    Review
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  7. Article
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  9. HMGB1: a multifaceted mediator of cell death pathways in cardiovascular diseases.Apoptosis : an international journal on programmed cell death · 2025
    Review
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  11. Involvement of role of HMGB1-NLRP3 pathway in systemic disorders.Frontiers in cell and developmental biology · 2025
    Review
  12. Article
  13. DAMP-ing IBD: Extinguish the Fire and Prevent Smoldering.Digestive diseases and sciences · 2025
    Review
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  15. Article
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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 1 institution in 1 country.

Eun Jung KimDepartment of Pharmacology, School of Medicine, Pusan National University, Yangsan, South Korea.
So Youn ParkDepartment of Pharmacology, School of Medicine, Pusan National University, Yangsan, South Korea.
Seung Eun BaekDepartment of Pharmacology, School of Medicine, Pusan National University, Yangsan, South Korea.
Min A JangDepartment of Pharmacology, School of Medicine, Pusan National University, Yangsan, South Korea.
Won Suk LeeDepartment of Pharmacology, School of Medicine, Pusan National University, Yangsan, South Korea.
Sun Sik BaeDepartment of Pharmacology, School of Medicine, Pusan National University, Yangsan, South Korea.
Koanhoi KimDepartment of Pharmacology, School of Medicine, Pusan National University, Yangsan, South Korea.
Chi Dae KimDepartment of Pharmacology, School of Medicine, Pusan National University, Yangsan, South Korea.
Pusan National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular smooth muscle cells (VSMCs) are the major cell type in the blood vessel walls, and their phenotypic modulation is a key cellular event driving vascular remodeling. Although high mobility group box-1 (HMGB1) plays a pivotal role in inflammatory processes after vascular injuries, the importance of the links between VSMCs, HMGB1 and vascular inflammation has not been clarified. To prove the hypothesis that VSMCs might be active players in vascular inflammation by secreting inflammatory cytokines, we investigated the proinflammatory effects of HMGB1 and its intermediary signaling pathways in VSMCs. When cultured human VSMCs were stimulated with HMGB1 (10-500 ng/ml), IL-1β production was markedly increased. HMGB1 also increased the expression of NLRP3 inflammasome components including NLRP3, ASC and caspase-1. Among these components, HMGB1-induced expressions of NLRP3 and caspase-1 were markedly attenuated in TLR2 siRNA-transfected cells, whereas ASC and caspase-1 expressions were reduced in RAGE-deficient cells. In TLR4-deficient cells, HMGB1-induced caspase-1 expression was significantly attenuated. Moreover, IL-1β production in HMGB1-stimulated cells was significantly reduced in cells transfected with caspase-1 siRNA as well as in cells treated with monoclonal antibodies or siRNAs for TLR2, TLR4 and RAGE. Overall, this study identified a pivotal role for NLRP3 inflammasome and its receptor signaling involved in the production of IL-1β in VSMCs stimulated with HMGB1. Thus, targeting HMGB1 signaling in VSMCs offers a promising therapeutic strategy for treating vascular remodeling diseases.

Indexed as

HMGB1IL-1βNLRP3 inflammasomeRAGETLRsVSMC

Identifiers

PMID29643819
PMCPMC5882820
OpenAlexW2794906623

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.