Evidence map›Paper›PMID 25644821›Full record

ArticleScientific reports2015

Angiotensin-converting enzyme 2/angiotensin-(1-7)/Mas axis prevents lipopolysaccharide-induced apoptosis of pulmonary microvascular endothelial cells by inhibiting JNK/NF-κB pathways.

Yingchuan Li, Yongmei Cao, Zhen Zeng, Mengfan Liang, Ying Xue, Caihua Xi, Ming Zhou, Wei Jiang

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

63 citing papers in PubMed, 106 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Anti-inflammatory effects ofFrontiers in pharmacology · 2025
    Article
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3 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Yingchuan LiDepartment of Anesthesiology, the Sixth People's Hospital Affiliated to Shanghai Jiaotong University, Shanghai 200233, China.
Yongmei CaoDepartment of Anesthesiology, the Sixth People's Hospital Affiliated to Shanghai Jiaotong University, Shanghai 200233, China.
Zhen ZengDepartment of Anesthesiology, the Sixth People's Hospital Affiliated to Shanghai Jiaotong University, Shanghai 200233, China.
Mengfan LiangDepartment of Anesthesiology, the Sixth People's Hospital Affiliated to Shanghai Jiaotong University, Shanghai 200233, China.
Ying XueDepartment of Anesthesiology, the Sixth People's Hospital Affiliated to Shanghai Jiaotong University, Shanghai 200233, China.
Caihua XiDepartment of Anesthesiology, the Sixth People's Hospital Affiliated to Shanghai Jiaotong University, Shanghai 200233, China.
Ming ZhouDepartment of Anesthesiology, the Sixth People's Hospital Affiliated to Shanghai Jiaotong University, Shanghai 200233, China.
Wei JiangDepartment of Anesthesiology, the Sixth People's Hospital Affiliated to Shanghai Jiaotong University, Shanghai 200233, China.
Shanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ACE2 and Ang-(1-7) have important roles in preventing acute lung injury. However, it is not clear whether upregulation of the ACE2/Ang-(1-7)/Mas axis prevents LPS-induced injury in pulmonary microvascular endothelial cells (PMVECs) by inhibiting the MAPKs/NF-κB pathways. Primary cultured rat PMVECs were transduced with lentiviral-borne Ace2 or shRNA-Ace2, and then treated or not with Mas receptor blocker (A779) before exposure to LPS. LPS stimulation resulted in the higher levels of AngII, Ang-(1-7), cytokine secretion, and apoptosis rates, and the lower ACE2/ACE ratio. Ace2 reversed the ACE2/ACE imbalance and increased Ang-(1-7) levels, thus reducing LPS-induced apoptosis and inflammation, while inhibition of Ace2 reversed all these effects. A779 abolished these protective effects of Ace2. LPS treatment was associated with activation of the ERK, p38, JNK, and NF-κB pathways, which were aggravated by A779. Pretreatment with A779 prevented the Ace2-induced blockade of p38, JNK, and NF-κB phosphorylation. However, only JNK inhibitor markedly reduced apoptosis and cytokine secretion in PMVECs with Ace2 deletion and A779 pretreatment. These results suggest that the ACE2/Ang-(1-7)/Mas axis has a crucial role in preventing LPS-induced apoptosis and inflammation of PMVECs, by inhibiting the JNK/NF-κB pathways.

Indexed as

Angiotensin-Converting Enzyme 2Angiotensin IAngiotensin IIAnimalsApoptosisCells, CulturedEndothelial CellsExtracellular Signal-Regulated MAP KinasesJNK Mitogen-Activated Protein KinasesLipopolysaccharidesLungMAP Kinase Signaling SystemMicrovesselsNF-kappa BPeptide FragmentsPeptidyl-Dipeptidase A7-Ala-angiotensin (1-7)Ace2 protein, ratAngiotensin-Converting Enzyme 2Angiotensin Iangiotensin I (1-7)Angiotensin IIExtracellular Signal-Regulated MAP KinasesJNK Mitogen-Activated Protein KinasesLipopolysaccharidesNF-kappa BPeptide FragmentsPeptidyl-Dipeptidase AProto-Oncogene MasProto-Oncogene ProteinsReceptors, G-Protein-CoupledRNA, Small Interfering

Identifiers

PMID25644821
PMCPMC4314638
OpenAlexW1981298734

What OpenQuestion 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 OpenQuestion graph.