Evidence map›Paper›PMID 29314607›Full record

ArticleJournal of cellular and molecular medicine2018

H3 relaxin inhibits the collagen synthesis via ROS- and P2X7R-mediated NLRP3 inflammasome activation in cardiac fibroblasts under high glucose.

Xiaohui Zhang, Yu Fu, Hui Li, Li Shen, Qing Chang, Liya Pan, Siting Hong, Xinhua Yin

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 4% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.

  1. Pooled it
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  9. Article
  10. Immune Fingerprint in Diabetes: Ocular Surface and Retinal Inflammation.International journal of molecular sciences · 2023
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. The Relaxin-3 Receptor, RXFP3, Is a Modulator of Aging-Related Disease.International journal of molecular sciences · 2022
    Review
  18. Possible roles of anti-type II collagen antibody and innate immunity in the development and progression of diabetic retinopathy.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2022
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Xiaohui ZhangThe Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Yu FuThe Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Hui LiThe Department of Cardiology, The Fifth hospital of Harbin, Harbin, China.
Li ShenThe Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Qing ChangThe Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Liya PanThe Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Siting HongThe Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Xinhua YinThe Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.ORCID 0000-0001-5096-6848
Harbin Medical University · CNWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excessive production of reactive oxygen species (ROS) and P2X7R activation induced by high glucose increases NLRP3 inflammasome activation, which contributes to the pathogenesis of diabetic cardiomyopathy. Although H3 relaxin has been shown to inhibit cardiac fibrosis induced by isoproterenol, the mechanism has not been well studied. Here, we demonstrated that high glucose (HG) induced the collagen synthesis by activation of the NLRP3 inflammasome, leading to caspase-1 activation, interleukin-1β (IL-1β) and IL-18 secretion in neonatal rat cardiac fibroblasts. Moreover, we used a high-glucose model with neonatal rat cardiac fibroblasts and showed that the activation of ROS and P2X7R was augmented and that ROS- and P2X7R-mediated NLRP3 inflammasome activation was critical for the collagen synthesis. Inhibition of ROS and P2X7R decreased NLRP3 inflammasome-mediated collagen synthesis, similar to the effects of H3 relaxin. Furthermore, H3 relaxin reduced the collagen synthesis via ROS- and P2X7R-mediated NLRP3 inflammasome activation in response to HG. These results provide a mechanism by which H3 relaxin alleviates NLRP3 inflammasome-mediated collagen synthesis through the inhibition of ROS and P2X7R under HG conditions and suggest that H3 relaxin represents a potential drug for alleviating cardiac fibrosis in diabetic cardiomyopathy.

Indexed as

AnimalsAnimals, NewbornCells, CulturedCollagenFemaleFibroblastsGlucoseInflammasomesInterleukin-18Interleukin-1betaMaleMyocardiumNLR Family, Pyrin Domain-Containing 3 ProteinRats, WistarReactive Oxygen SpeciesReceptors, Purinergic P2X7CollagenGlucoseInflammasomesInterleukin-18Interleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesReceptors, Purinergic P2X7Relaxincardiac fibrosishigh glucoseNLRP3 inflammasomeP2X7RROS

Identifiers

PMID29314607
PMCPMC5824385
OpenAlexW4244851433

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.