Evidence map›Paper›PMID 31883300›Full record

ArticleJournal of cellular and molecular medicine2020

NFAT5 promotes arteriogenesis via MCP-1-dependent monocyte recruitment.

Xing-Chi Lin, Miao Pan, Ling-Ping Zhu, Quan Sun, Zheng-Shi Zhou, Chuan-Chang Li, Guo-Gang Zhang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. 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
1.4field-weighted citation impact, top 16% 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, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Role of Vascular Smooth Muscle Cell Phenotype Switching in Arteriogenesis.International journal of molecular sciences · 2021
    Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. NFAT5 promotes arteriogenesis via MCP-1-dependent monocyte recruitment.Journal of cellular and molecular medicine · 2020
    Article
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

7 authors at 1 institution in 1 country.

Xing-Chi LinDepartment of Cardiovascular Medicine, Xiangya Hospital, Central South University, Changsha, China.
Miao PanDepartment of Cardiovascular Medicine, Xiangya Hospital, Central South University, Changsha, China.
Ling-Ping ZhuDepartment of Cardiovascular Medicine, Xiangya Hospital, Central South University, Changsha, China.
Quan SunDepartment of Cardiovascular Medicine, Xiangya Hospital, Central South University, Changsha, China.
Zheng-Shi ZhouDepartment of Laboratory Animal, Xiangya School of Medicine, Central South University, Changsha, China.
Chuan-Chang LiDepartment of Geriatric Medicine, Xiangya Hospital, Central South University, Changsha, China.
Guo-Gang ZhangDepartment of Cardiovascular Medicine, Xiangya Hospital, Central South University, Changsha, China.ORCID 0000-0002-8678-2167
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Studies have demonstrated that nuclear factor of activated T cells 5 (NFAT5) is not only a tonicity-responsive transcription factor but also activated by other stimuli, so we aim to investigate whether NFAT5 participates in collateral arteries formation in rats. We performed femoral artery ligature (FAL) in rats for hindlimb ischaemia model and found that NFAT5 was up-regulated in rat adductors with FAL compared with sham group. Knockdown of NFAT5 with locally injection of adenovirus-mediated NFAT5-shRNA in rats significantly inhibited hindlimb blood perfusion recovery and arteriogenesis. Moreover, NFAT5 knockdown decreased macrophages infiltration and monocyte chemotactic protein-1 (MCP-1) expression in rats adductors. In vitro, with interleukin-1β (IL-1β) stimulation and loss-of-function studies, we demonstrated that NFAT5 knockdown inhibits MCP-1 expression in endothelial cells and chemotaxis of THP-1 cells regulated by ERK1/2 pathway. More importantly, exogenous MCP-1 delivery could recover hindlimb blood perfusion, promote arteriogenesis and macrophages infiltration in rats after FAL, which were depressed by NFAT5 knockdown. Besides, NFAT5 knockdown also inhibited angiogenesis in gastrocnemius muscles in rats. Our results indicate that NFAT5 is a critical regulator of arteriogenesis and angiogenesis via MCP-1-dependent monocyte recruitment, suggesting that NFAT5 may represent an alternative therapeutic target for ischaemic diseases.

Indexed as

OrganogenesisAnimalsArteriesCell NucleusChemokine CCL2ChemotaxisCollateral CirculationDisease Models, AnimalGene Knockdown TechniquesHindlimbHumansHuman Umbilical Vein Endothelial CellsInterleukin-1betaIschemiaMaleMAP Kinase Signaling SystemChemokine CCL2Interleukin-1betaNFAT5 protein, humanNfat5 protein, ratTranscription Factorsarteriogenesishindlimb ischaemiamacrophagemonocyte chemoattractant protein 1nuclear factor of activated T cells 5

Identifiers

PMID31883300
PMCPMC6991654
OpenAlexW2998618859

What OpenQuestion holds

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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.