Evidence map›Paper›PMID 33318302›Full record

ArticleAging2020

TLR2 regulates angiotensin II-induced vascular remodeling and EndMT through NF-κB signaling.

Ke Lin, Wu Luo, Jueqian Yan, Siyuan Shen, Qirui Shen, Jun Wang, Xinfu Guan, Gaojun Wu, Weijian Huang, Guang Liang

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Immune and Metabolic Mechanisms of Endothelial Dysfunction.International journal of molecular sciences · 2024
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. IdentifyingFrontiers in cardiovascular medicine · 2024
    Article
  12. Review
  13. Article
  14. Vascular Stress Signaling in Hypertension.Circulation research · 2021
    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

10 authors at 2 institutions in 1 country.

Ke LinChemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325035, Zhejiang, China.
Wu LuoChemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325035, Zhejiang, China.
Jueqian YanChemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325035, Zhejiang, China.
Siyuan ShenChemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325035, Zhejiang, China.
Qirui ShenChemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325035, Zhejiang, China.
Jun WangDepartment of Cardiology, Wenzhou Central Hospital and Affiliated Dingli Clinical Institute, Wenzhou Medical University, Wenzhou 325035, Zhejiang, China.
Xinfu GuanAffiliated Cangnan Hospital, Wenzhou Medical University, Cangnan 325800, Zhejiang, China.
Gaojun WuDepartment of Cardiology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325035, Zhejiang, China.
Weijian HuangDepartment of Cardiology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325035, Zhejiang, China.
Guang LiangChemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325035, Zhejiang, China.
Wenzhou Medical University · CNFirst Affiliated Hospital of Wenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excessive vascular remodeling has been shown in hypertensive patients. In experimental models of hypertensive vascular injury, such as angiotensin II (Ang II) challenged mice, toll like receptor 2 (TLR2) initiates inflammatory responses. More recently, studies have reported atypical endothelial to mesenchymal transition (EndMT) in vascular injuries and inflammatory conditions. Here, we aimed to investigate whether TLR2 mediates Ang II-induced vascular inflammation and initiates EndMT. In a mouse model of angiotensin II-induced hypertension, we show that aortas exhibit increased medial thickening, fibrosis, and features of EndMT. These alterations were not observed in TLR2 knockout mice in response to Ang II. TLR2 silencing in cultured endothelial cells confirmed the essential role of TLR2 in Ang II-induced inflammatory factor induction, and EndMT-associated phenotypic change. Mechanistically, we found Ang II activates nuclear factor-κB signaling, inducing pro-inflammatory cytokine production, and mediates EndMT in both cultured endothelial cells and in mice. These studies illustrate a novel role of TLR2 in regulating Ang II-induced deleterious vascular remodeling through the induction of EndMT. The studies also suggest that TLR2 may be targeted to alleviate hypertension-associated vascular injury.

Indexed as

Angiotensin IIAnimalsAortaEndothelial CellsFibrosisHumansHuman Umbilical Vein Endothelial CellsMiceMice, KnockoutNF-kappa BSignal TransductionToll-Like Receptor 2Vascular RemodelingAngiotensin IINF-kappa BToll-Like Receptor 2angiotensin IIendothelial to mesenchymal transitionNF-κBTLR2vascular remodeling

Identifiers

PMID33318302
PMCPMC7880316
OpenAlexW3112456915

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.