Evidence map›Paper›PMID 36613682›Full record

ReviewInternational journal of molecular sciences2022

Inhibitors of the Sialidase NEU3 as Potential Therapeutics for Fibrosis.

Tejas R Karhadkar, Wensheng Chen, Darrell Pilling, Richard H Gomer

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Degradation System: Sialidase.Methods in molecular biology (Clifton, N.J.) · 2026
    Article
  3. Review
  4. Article
  5. Acute and Subacute Toxicity of Sialidase FromVeterinary medicine international · 2025
    Article
  6. Review
  7. Review
  8. Review
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

4 authors at 1 institution in 1 country.

Tejas R KarhadkarDepartment of Biology, Texas A&M University, College Station, TX 77843-3474, USA.
Wensheng ChenDepartment of Biology, Texas A&M University, College Station, TX 77843-3474, USA.ORCID 0000-0002-2853-8422
Darrell PillingDepartment of Biology, Texas A&M University, College Station, TX 77843-3474, USA.ORCID 0000-0002-7413-2773
Richard H GomerDepartment of Biology, Texas A&M University, College Station, TX 77843-3474, USA.
Texas A&M University · US

Funding

Breaking a novel feedback loop to inhibit fibrosisR01HL132919 · NHLBI · TEXAS A&M UNIVERSITY · PI GOMER, RICHARD H · 2018 to 2021
$1.4M
NHLBI NIH HHS R01 HL132919NIH HHS R01 HL132919
6 · The paper itself

Abstract

Fibrosing diseases are a major medical problem, and are associated with more deaths per year than cancer in the US. Sialidases are enzymes that remove the sugar sialic acid from glycoconjugates. In this review, we describe efforts to inhibit fibrosis by inhibiting sialidases, and describe the following rationale for considering sialidases to be a potential target to inhibit fibrosis. First, sialidases are upregulated in fibrotic lesions in humans and in a mouse model of pulmonary fibrosis. Second, the extracellular sialidase NEU3 appears to be both necessary and sufficient for pulmonary fibrosis in mice. Third, there exist at least three mechanistic ways in which NEU3 potentiates fibrosis, with two of them being positive feedback loops where a profibrotic cytokine upregulates NEU3, and the upregulated NEU3 then upregulates the profibrotic cytokine. Fourth, a variety of NEU3 inhibitors block pulmonary fibrosis in a mouse model. Finally, the high sialidase levels in a fibrotic lesion cause an easily observed desialylation of serum proteins, and in a mouse model, sialidase inhibitors that stop fibrosis reverse the serum protein desialylation. This then indicates that serum protein sialylation is a potential surrogate biomarker for the effect of sialidase inhibitors, which would facilitate clinical trials to test the exciting possibility that sialidase inhibitors could be used as therapeutics for fibrosis.

Indexed as

Pulmonary FibrosisAnimalsCytokinesGlycoconjugatesHumansMiceN-Acetylneuraminic AcidNeuraminidaseCytokinesGlycoconjugatesN-Acetylneuraminic AcidNeu3 protein, humanNeu3 protein, mouseNeuraminidasebiomarkerdesialylationidiopathic pulmonary fibrosisneuraminidasepentraxinserum amyloid Psialylationtransforming growth factor

Identifiers

PMID36613682
PMCPMC9820515
OpenAlexW4312175618

What OpenQuestion holds

Textmetadata
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.