Evidence map›Paper›PMID 33527026›Full record

ArticleAmerican journal of translational research2021

TLR4 regulates vascular smooth muscle cell proliferation in hypertension via modulation of the NLRP3 inflammasome.

Hui-Meng Qi, Qin Cao, Qiang Liu

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.6field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Vessel-On-A-Chip Coupled Proteomics Reveal Pressure-Overload-Induced Vascular Remodeling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. NLRP3 inflammasome: The rising star in cardiovascular diseases.Frontiers in cardiovascular medicine · 2022
    Review
  15. Article
  16. O-Linked β-Frontiers in immunology · 2022
    Review
  17. Review
  18. Review
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

3 authors at 1 institution in 1 country.

Hui-Meng QiDepartment of General Practice, The First Hospital of China Medical University Shenyang, China.
Qin CaoDepartment of Gastroenterolog, The First Hospital of China Medical University Shenyang, China.
Qiang LiuDepartment of Nephrology, The First Hospital of China Medical University Shenyang, China.
China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Backgroud: Toll-like receptor 4 (TLR4), a key mediator of inflammatory responses, which is associated with vascular remodeling. The association between TLR4 and NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome in the regulation of vascular smooth muscle cell (VSMC) proliferation remains unclear. This study was to explore the role and underlying mechanisms of TLR4 in the proliferation of VSMC in hypertension.

methodsVSMC proliferation after TLR4 overexpression or downregulation was determined by CCK-8, EdU Incorporation and colony formation assays. Western blots were carried out to investigate the expression of TLR4 and NLRP3 inflammasome components in VSMCs. Next, blood pressure measurements and Hematoxylin and Eosin (HE) staining assays were performed in spontaneously hypertensive rats (SHR). Media thickness (M) and diameter lumen (L) were measured as indicators of vascular remodeling. The expression of TLR4, PCNA and NLRP3 inflammasome complex was analyzed by Western blots in the aorta of SHR.

resultsWe showed that TLR4 overexpression with cDNA enhanced, while knockdown of TLR4 with shRNA inhibited Ang II-induced VSMC proliferation. Besides, TLR4 overexpression upregulated the proteion expression of the NLRP3 inflammasome components including NLRP3, ASC and caspase-1, whereas their corresponding levels of expression were observed to decrease in TLR4 shRNA-transfected VSMCs. Knockdown of TLR4 attenuated vascular remodeling, blood pressure (BP) and the levels of NLRP3, ASC, caspase-1, IL-1β and IL-18 in SHR aortas.

conclusionThis study revealed that TLR4 regulated Ang II-induced VSMC proliferation through modulating the NLRP3 inflammasome. Knockdown of TLR4 attenuated the BP and vascular remodeling by inhibiting the expression of the NLRP3 inflammasome component in SHR. Our results support that TLR4 regulates VSMC proliferation in hypertension via triggering the NLRP3 inflammasome.

Indexed as

hypertensionNLRP3 inflammasomeproliferationTLR4

Identifiers

PMID33527026
PMCPMC7847527
OpenAlexW3126551041

What Socratic 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 Socratic graph.