Evidence map›Paper›PMID 31250885›Full record

ArticleCardiovascular research2020

Chanzyme TRPM7 protects against cardiovascular inflammation and fibrosis.

Francisco J Rios, Zhi-Guo Zou, Adam P Harvey, Katie Y Harvey, Ryszard Nosalski, Panagiota Anyfanti, Livia L Camargo, Silvia Lacchini, Alexey G Ryazanov, Lillia Ryazanova and 5 more

Registry-linked trialOpen access · hybridAbstract read
In one paragraph

Article in Cardiovascular research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06726460 (Validation of the Accuracy of a Novel POCT Dry Electrolyte Analysis System in the Acute Care Setting), which is not on this map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
8.5field-weighted citation impact, top 1% 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.

NCT06726460 recruitingnot on this mapstarted 2024, after this paper: background citation

Validation of the Accuracy of a Novel POCT Dry Electrolyte Analysis System in the Acute Care Setting: A Cross-Sectional Study

TypeobservationalSponsorZhujiang HospitalRan2024 to 2025Enrolled200ConditionsElectrolyte Disorder, Arrhythmia, StrokeArmsNova Stat Profile pHOx Ultra Analyzer System(Nova), Novel POCT dry electrolyte analysis system(P1)
3 · Its place in the literature

Who cites it

61 citing papers in PubMed, 104 citations in OpenAlex.

  1. Article
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  8. IL-6 Does Not Influence the Expression ofInternational journal of molecular sciences · 2024
    Article
  9. Review
  10. Article
  11. Article
  12. TRPM channels in health and disease.Nature reviews. Nephrology · 2024
    Review
  13. Article
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  15. Article
  16. Review
  17. Article
  18. Article
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1 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 5 institutions in 4 countries.

Francisco J RiosInstitute of Cardiovascular and Medical Sciences, BHF Glasgow Cardiovascular Research Centre, University of Glasgow, 126 University Place, Glasgow G12 8TA, UK.
Zhi-Guo ZouInstitute of Cardiovascular and Medical Sciences, BHF Glasgow Cardiovascular Research Centre, University of Glasgow, 126 University Place, Glasgow G12 8TA, UK.
Adam P HarveyInstitute of Cardiovascular and Medical Sciences, BHF Glasgow Cardiovascular Research Centre, University of Glasgow, 126 University Place, Glasgow G12 8TA, UK.
Katie Y HarveyInstitute of Cardiovascular and Medical Sciences, BHF Glasgow Cardiovascular Research Centre, University of Glasgow, 126 University Place, Glasgow G12 8TA, UK.
Ryszard NosalskiInstitute of Cardiovascular and Medical Sciences, BHF Glasgow Cardiovascular Research Centre, University of Glasgow, 126 University Place, Glasgow G12 8TA, UK.
Panagiota Anyfanti3rd Department of Internal Medicine, Papageorgiou Hospital, Aristotle University of Thessaloniki, Thessaloniki, Greece.
Livia L CamargoInstitute of Cardiovascular and Medical Sciences, BHF Glasgow Cardiovascular Research Centre, University of Glasgow, 126 University Place, Glasgow G12 8TA, UK.
Silvia LacchiniDepartment of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, São Paulo, Brazil.
Alexey G RyazanovDepartment of Pharmacology, Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ, USA.
Lillia RyazanovaLewis Sigler Institute of Integrative Genomics, Princeton University, Princeton, NJ, USA.
Sarah McGrathCentre of Immunobiology, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK.
Tomasz J GuzikInstitute of Cardiovascular and Medical Sciences, BHF Glasgow Cardiovascular Research Centre, University of Glasgow, 126 University Place, Glasgow G12 8TA, UK.
Carl S GoodyearCentre of Immunobiology, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK.
Augusto C MontezanoInstitute of Cardiovascular and Medical Sciences, BHF Glasgow Cardiovascular Research Centre, University of Glasgow, 126 University Place, Glasgow G12 8TA, UK.
Rhian M TouyzInstitute of Cardiovascular and Medical Sciences, BHF Glasgow Cardiovascular Research Centre, University of Glasgow, 126 University Place, Glasgow G12 8TA, UK.
University of Glasgow · GBAristotle University of Thessaloniki · GRPrinceton University · USRutgers, The State University of New Jersey · USUniversidade de São Paulo · BR

Funding

British Heart Foundation CH/4/29762British Heart Foundation RE/13/5/30177British Heart Foundation RG/13/7/30099Medical Research Council 171319-06Medical Research Council MC_PC_14133
6 · The paper itself

Abstract

aimsTransient Receptor Potential Melastatin 7 (TRPM7) cation channel is a chanzyme (channel + kinase) that influences cellular Mg2+ homeostasis and vascular signalling. However, the pathophysiological significance of TRPM7 in the cardiovascular system is unclear. The aim of this study was to investigate the role of this chanzyme in the cardiovascular system focusing on inflammation and fibrosis. METHODS AND

resultsTRPM7-deficient mice with deletion of the kinase domain (TRPM7+/Δkinase) were studied and molecular mechanisms investigated in TRPM7+/Δkinase bone marrow-derived macrophages (BMDM) and co-culture systems with cardiac fibroblasts. TRPM7-deficient mice had significant cardiac hypertrophy, fibrosis, and inflammation. Cardiac collagen and fibronectin content, expression of pro-inflammatory mediators (SMAD3, TGFβ) and cytokines [interleukin (IL)-6, IL-10, IL-12, tumour necrosis factor-α] and phosphorylation of the pro-inflammatory signalling molecule Stat1, were increased in TRPM7+/Δkinase mice. These processes were associated with infiltration of inflammatory cells (F4/80+CD206+ cardiac macrophages) and increased galectin-3 expression. Cardiac [Mg2+]i, but not [Ca2+]i, was reduced in TRPM7+/Δkinase mice. Calpain, a downstream TRPM7 target, was upregulated (increased expression and activation) in TRPM7+/Δkinase hearts. Vascular functional and inflammatory responses, assessed in vivo by intra-vital microscopy, demonstrated impaired neutrophil rolling, increased neutrophil: endothelial attachment and transmigration of leucocytes in TRPM7+/Δkinase mice. TRPM7+/Δkinase BMDMs had increased levels of galectin-3, IL-10, and IL-6. In co-culture systems, TRPM7+/Δkinase macrophages increased expression of fibronectin, proliferating cell nuclear antigen, and TGFβ in cardiac fibroblasts from wild-type mice, effects ameliorated by MgCl2 treatment.

conclusionsWe identify a novel anti-inflammatory and anti-fibrotic role for TRPM7 and suggest that its protective effects are mediated, in part, through Mg2+-sensitive processes.

Indexed as

Ventricular RemodelingAnimalsCardiomegalyCardiomyopathiesCell ProliferationCells, CulturedCoculture TechniquesFibroblastsFibrosisInflammationInflammation MediatorsLeukocyte RollingMacrophagesMagnesiumMaleMice, 129 StrainInflammation MediatorsMagnesiumTrpm7 protein, mouseTRPM Cation ChannelsCardiac hypertrophyCationsMagnesium channelVascular inflammation

Identifiers

PMID31250885
PMCPMC7252442
OpenAlexW2955332689

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LicenceCC BY
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Registered trials

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.