Evidence map›Paper›PMID 32899668›Full record

ReviewInternational journal of molecular sciences2020

Interleukin-36 Cytokine/Receptor Signaling: A New Target for Tissue Fibrosis.

Elaina Melton, Hongyu Qiu

Registry-linked trialAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05775107 (Assessment of Pancreatic Fibrosis as a Prognostic Factor of Its Course), which is not on this map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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.

NCT05775107 unknown statusnot on this mapstarted 2022, after this paper: background citation

Assessment of Pancreatic Fibrosis as a Prognostic Factor of Its Course

TypeobservationalSponsorMoscow Clinical Scientific CenterRan2022 to 2025Enrolled150ConditionsPancreatic Fibrosis
3 · Its place in the literature

Who cites it

15 citing papers in PubMed.

  1. Article
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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

2 authors.

Elaina MeltonCenter for Molecular and Translational Medicine, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA 30303, USA.ORCID 0000-0002-4030-7766
Hongyu QiuCenter for Molecular and Translational Medicine, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA 30303, USA.

Funding

Intrinsic Stiffness of Aortic Vascular Smooth Muscle Cell in the Development of HypertensionR01HL115195 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI QIU, HONGYU · 2013 to 2022
$5.1M
Role of VCP in coronary ischemic injuryR01HL142291 · NHLBI · LOMA LINDA UNIVERSITY · PI QIU, HONGYU, XIE, ZHONGLIN · 2018 to 2021
$2.6M
Novel mechanism mediating cardiac protection upon pressure overloadR01HL137962 · NHLBI · LOMA LINDA UNIVERSITY · PI QIU, HONGYU · 2018 to 2020
$1.2M
Novel mechanisms mediating cardiac protection upon pressure overloadR56HL137962 · NHLBI · LOMA LINDA UNIVERSITY · PI QIU, HONGYU · 2017 to 2017
$393k
NHLBI NIH HHS R01 HL115195NHLBI NIH HHS R01 HL137962NHLBI NIH HHS R01 HL142291NHLBI NIH HHS R56 HL137962NIH HHS HL115195-01; HL137962 and HL 142291
6 · The paper itself

Abstract

Tissue fibrosis is a major unresolved medical problem, which impairs the function of various systems. The molecular mechanisms involved are poorly understood, which hinders the development of effective therapeutic strategies. Emerging evidence from recent studies indicates that interleukin 36 (IL-36) and the corresponding receptor (IL-36R), a newly-characterized cytokine/receptor signaling complex involved in immune-inflammation, play an important role in the pathogenesis of fibrosis in multiple tissues. This review focuses on recent experimental findings, which implicate IL-36R and its associated cytokines in different forms of organ fibrosis. Specifically, it outlines the molecular basis and biological function of IL-36R in normal cells and sums up the pathological role in the development of fibrosis in the lung, kidney, heart, intestine, and pancreas. We also summarize the new progress in the IL-36/IL-36R-related mechanisms involved in tissue fibrosis and enclose the potential of IL-36R inhibition as a therapeutic strategy to combat pro-fibrotic pathologies. Given its high association with disease, gaining new insight into the immuno-mechanisms that contribute to tissue fibrosis could have a significant impact on human health.

Indexed as

CytokinesFibrosisHumansInflammationInterleukin-1InterleukinsReceptors, Interleukin-1Signal TransductionCytokinesInterleukin-1interleukin 36, humanInterleukinsReceptors, Interleukin-1IL-1 receptor familyIL-36IL-36RIL-38inflammationtissue fibrosis

Identifiers

PMID32899668
PMCPMC7556029

What OpenQuestion holds

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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.