Evidence map›Paper›PMID 28981106›Full record

ArticleCell death & disease2017

NLRP3 inflammasome activation contributes to VSMC phenotypic transformation and proliferation in hypertension.

Hai-Jian Sun, Xing-Sheng Ren, Xiao-Qing Xiong, Yun-Zhi Chen, Ming-Xia Zhao, Jue-Jin Wang, Ye-Bo Zhou, Ying Han, Qi Chen, Yue-Hua Li and 2 more

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07206303 (The Effects of Bifidobacterium-based Probiotics in Reducing Blood Pressure in Middle-aged Chinese With Hypertension), which is not on this map. Cited by 142 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
142citing papers in PubMed, 1 pooled it
7.4field-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.

NCT07206303 phase1not yet recruitingnot on this mapstarted 2026, after this paper: background citation

The Effects of Bifidobacterium-based Probiotics in Reducing Blood Pressure in Middle-aged Chinese With Hypertension: a Single-term Feasibility Pilot Study

TypeinterventionalSponsorThe University of Hong KongRan2026 to 2027Enrolled30ConditionsHypertensionArmsBifidobacterium probiotics supplementation
3 · Its place in the literature

Who cites it

142 citing papers in PubMed, 1 synthesis or guideline pooled it, 237 citations in OpenAlex.

  1. Pooled it
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  3. 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
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82 more citing papers are in PubMed but not listed here.

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

12 authors at 3 institutions in 1 country.

Hai-Jian SunDepartment of Physiology, Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University, Nanjing, Jiangsu 210029, China.
Xing-Sheng RenDepartment of Physiology, Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University, Nanjing, Jiangsu 210029, China.
Xiao-Qing XiongDepartment of Physiology, Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University, Nanjing, Jiangsu 210029, China.
Yun-Zhi ChenDepartment of Physiology, Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University, Nanjing, Jiangsu 210029, China.
Ming-Xia ZhaoDepartment of Physiology, Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University, Nanjing, Jiangsu 210029, China.
Jue-Jin WangDepartment of Physiology, Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University, Nanjing, Jiangsu 210029, China.
Ye-Bo ZhouDepartment of Physiology, Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University, Nanjing, Jiangsu 210029, China.
Ying HanDepartment of Physiology, Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University, Nanjing, Jiangsu 210029, China.
Qi ChenDepartment of Pathophysiology, Nanjing Medical University, Nanjing, Jiangsu 210029, China.
Yue-Hua LiDepartment of Pathophysiology, Nanjing Medical University, Nanjing, Jiangsu 210029, China.
Yu-Ming KangDepartment of Physiology and Pathophysiology, Cardiovascular Research Center, Xi'an Jiaotong University School of Medicine, Xi'an, Shanxi 710061, China.
Guo-Qing ZhuDepartment of Physiology, Key Laboratory of Cardiovascular Disease and Molecular Intervention, Nanjing Medical University, Nanjing, Jiangsu 210029, China.ORCID 0000-0002-3132-9592
Nanjing Medical University · CNJiangnan University · CNXi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation is involved in pathogenesis of hypertension. NLRP3 inflammasome activation is a powerful mediator of inflammatory response via caspase-1 activation. The present study was designed to determine the roles and mechanisms of NLRP3 inflammasome in phenotypic modulation and proliferation of vascular smooth muscle cells (VSMCs) in hypertension. Experiments were conducted in spontaneously hypertensive rats (SHR) and primary aortic VSMCs. NLRP3 inflammasome activation was observed in the media of aorta in SHR and in the VSMCs from SHR. Knockdown of NLRP3 inhibited inflammasome activation, VSMC phenotypic transformation and proliferation in SHR-derived VSMCs. Increased NFκB activation, histone acetylation and histone acetyltransferase expression were observed in SHR-derived VSMCs and in media of aorta in SHR. Chromatin immunoprecipitation analysis revealed the increased histone acetylation, p65-NFκB and Pol II occupancy at the NLRP3 promoter in vivo and in vitro. Inhibition of NFκB with BAY11-7082 or inhibition of histone acetyltransferase with curcumin prevented the NLRP3 inflammasome activation, VSMC phenotype switching and proliferation in VSMCs from SHR. Moreover, curcumin repressed NFκB activation. Silencing of NLRP3 gene ameliorated hypertension, vascular remodeling, NLRP3 inflammasome activation and phenotype switching in the aorta of SHR. These results indicate that NLRP3 inflammasome activation response to histone acetylation and NFκB activation contributes to VSMC phenotype switching and proliferation and vascular remodeling in hypertension.

Indexed as

Angiotensin IIAnimalsCaspase 1Cell ProliferationCurcuminGene Expression RegulationHumansHypertensionInflammasomesMuscle, Smooth, VascularNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinPhenotypeRatsRats, Inbred SHRSignal TransductionAngiotensin IICaspase 1CurcuminInflammasomesNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, rat

Identifiers

PMID28981106
PMCPMC5680591
OpenAlexW2762325358

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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 Socratic graph.