Evidence map›Paper›PMID 37340199›Full record

ArticleCellular and molecular life sciences : CMLS2023

Macrophage Dectin-1 mediates Ang II renal injury through neutrophil migration and TGF-β1 secretion.

Shiju Ye, He Huang, Yun Xiao, Xue Han, Fengjie Shi, Wu Luo, Jiawen Chen, Yang Ye, Xia Zhao, Weijian Huang and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

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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

14 authors at 3 institutions in 1 country.

Shiju Ye *Key Laboratory of Cardiovascular Intervention and Regenerative Medicine of Zhejiang Province, Department of Cardiology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, 310020, Zhejiang, China.
He Huang *Key Laboratory of Cardiovascular Intervention and Regenerative Medicine of Zhejiang Province, Department of Cardiology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, 310020, Zhejiang, China.
Yun Xiao *Key Laboratory of Cardiovascular Intervention and Regenerative Medicine of Zhejiang Province, Department of Cardiology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, 310020, Zhejiang, China.
Xue HanSchool of Pharmaceutical Sciences, Hangzhou Medical College, Hangzhou, 311399, Zhejiang, China.
Fengjie ShiKey Laboratory of Cardiovascular Intervention and Regenerative Medicine of Zhejiang Province, Department of Cardiology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, 310020, Zhejiang, China.
Wu LuoSchool of Pharmaceutical Sciences, Hangzhou Medical College, Hangzhou, 311399, Zhejiang, China.
Jiawen ChenKey Laboratory of Cardiovascular Intervention and Regenerative Medicine of Zhejiang Province, Department of Cardiology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, 310020, Zhejiang, China.
Yang YeKey Laboratory of Cardiovascular Intervention and Regenerative Medicine of Zhejiang Province, Department of Cardiology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, 310020, Zhejiang, China.
Xia ZhaoSchool of Pharmaceutical Sciences, Hangzhou Medical College, Hangzhou, 311399, Zhejiang, China.
Weijian HuangDepartment of Cardiology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China.
Yi WangChemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China.
Dongwu LaiKey Laboratory of Cardiovascular Intervention and Regenerative Medicine of Zhejiang Province, Department of Cardiology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, 310020, Zhejiang, China.
Guang LiangSchool of Pharmaceutical Sciences, Hangzhou Medical College, Hangzhou, 311399, Zhejiang, China. wzmcliangguang@163.com.
Guosheng FuKey Laboratory of Cardiovascular Intervention and Regenerative Medicine of Zhejiang Province, Department of Cardiology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, 310020, Zhejiang, China. fugs@zju.edu.cn.ORCID http://orcid.org/0000-0001-7027-0717
Sir Run Run Shaw Hospital · CNWenzhou Medical University · CNHangzhou Medical College · CN

Funding

National Key Research Project 2017YFA0506000National Natural Science Foundation of China 81930108National Natural Science Foundation of China 82000224National Natural Science Foundation of China 82000793National Natural Science Foundation of China 82070359
6 · The paper itself

Abstract

Macrophage activation has been shown to play an essential role in renal fibrosis and dysfunction in hypertensive chronic kidney disease. Dectin-1 is a pattern recognition receptor that is also involved in chronic noninfectious diseases through immune activation. However, the role of Dectin-1 in Ang II-induced renal failure is still unknown. In this study, we found that Dectin-1 expression on CD68 + macrophages was significantly elevated in the kidney after Ang II infusion. We assessed the effect of Dectin-1 on hypertensive renal injury using Dectin-1-deficient mice infused by Angiotensin II (Ang II) at 1000 ng/kg/min for 4 weeks. Ang II-induced renal dysfunction, interstitial fibrosis, and immune activation were significantly attenuated in Dectin-1-deficient mice. A Dectin-1 neutralizing antibody and Syk inhibitor (R406) were used to examine the effect and mechanism of Dectin-1/Syk signaling axle on cytokine secretion and renal fibrosis in culturing cells. Blocking Dectin-1 or inhibiting Syk significantly reduced the expression and secretion of chemokines in RAW264.7 macrophages. The in vitro data showed that the increase in TGF-β1 in macrophages enhanced the binding of P65 and its target promotor via the Ang II-induced Dectin-1/Syk pathway. Secreted TGF-β1 caused renal fibrosis in kidney cells through Smad3 activation. Thus, macrophage Dectin-1 may be involved in the activation of neutrophil migration and TGF-β1 secretion, thereby promoting kidney fibrosis and dysfunction.

Indexed as

Angiotensin IIHypertension, RenalAnimalsDectin-1FibrosisKidneyMacrophagesMiceNeutrophilsTransforming Growth Factor beta1Angiotensin IIDectin-1Transforming Growth Factor beta1Angiotensin IIChronic kidney diseaseDectin-1HypertensionTGF-β1

Identifiers

PMID37340199
PMCPMC10282045
OpenAlexW4381332526

What OpenQuestion holds

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LicenceCC BY
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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.