Evidence map›Paper›PMID 24695531›Full record

ArticlePloS one2014

Persistent lung inflammation and fibrosis in serum amyloid P component (APCs-/-) knockout mice.

Darrell Pilling, Richard H Gomer

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

49 citing papers in PubMed, 78 citations in OpenAlex.

  1. First-in-Human Phase I/II Study of NEOD001 in Patients With Light Chain Amyloidosis and Persistent Organ Dysfunction.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2016
    Trial
  2. Article
  3. Article
  4. Article
  5. Emerging Concepts in Therapeutic Interventions for Idiopathic Pulmonary Fibrosis.Seminars in respiratory and critical care medicine · 2025
    Review
  6. Article
  7. Article
  8. Review
  9. Serum amyloid P component (SAP) modulates antidepressant effects through promoting membrane insertion of the serotonin transporter.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
    Article
  10. Article
  11. Article
  12. Inhibitors of the Sialidase NEU3 as Potential Therapeutics for Fibrosis.International journal of molecular sciences · 2022
    Review
  13. The extracellular sialidase NEU3 primes neutrophils.Journal of leukocyte biology · 2022
    Article
  14. Article
  15. Idiopathic pulmonary fibrosis: Current and future treatment.The clinical respiratory journal · 2022
    Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Inhibiting Sialidase-Induced TGF-The Journal of pharmacology and experimental therapeutics · 2021
    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

2 authors at 1 institution in 1 country.

Darrell PillingDepartment of Biology, Texas A&M University, College Station, Texas, United States of America.
Richard H GomerDepartment of Biology, Texas A&M University, College Station, Texas, United States of America.
Texas A&M University · US

Funding

Regulating fibrocyte differentiation in fibrosisR01HL083029 · NHLBI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI GOMER, RICHARD H · 2006 to 2009
$1.5M
Pentraxin regulation of macrophage differentiationR01HL118507 · NHLBI · TEXAS A&M UNIVERSITY · PI GOMER, RICHARD H · 2014 to 2017
$1.4M
NHLBI NIH HHS HL083029NHLBI NIH HHS R01 HL083029NHLBI NIH HHS R01 HL118507
6 · The paper itself

Abstract

Fibrosing diseases, such as pulmonary fibrosis, cardiac fibrosis, myelofibrosis, liver fibrosis, and renal fibrosis are chronic and debilitating conditions and are an increasing burden for the healthcare system. Fibrosis involves the accumulation and differentiation of many immune cells, including macrophages and fibroblast-like cells called fibrocytes. The plasma protein serum amyloid P component (SAP; also known as pentraxin-2, PTX2) inhibits fibrocyte differentiation in vitro, and injections of SAP inhibit fibrosis in vivo. SAP also promotes the formation of immuno-regulatory Mreg macrophages. To elucidate the endogenous function of SAP, we used bleomycin aspiration to induce pulmonary inflammation and fibrosis in mice lacking SAP. Compared to wildtype C57BL/6 mice, we find that in Apcs-/- "SAP knock-out" mice, bleomycin induces a more persistent inflammatory response and increased fibrosis. In both C57BL/6 and Apcs-/- mice, injections of exogenous SAP reduce the accumulation of inflammatory macrophages and prevent fibrosis. The types of inflammatory cells present in the lungs following bleomycin-aspiration appear similar between C57BL/6 and Apcs-/- mice, suggesting that the initial immune response is normal in the Apcs-/- mice, and that a key endogenous function of SAP is to promote the resolution of inflammation and fibrosis.

Indexed as

AnimalsBleomycinCell DifferentiationLungMiceMice, Inbred C57BLMice, KnockoutPneumoniaPulmonary FibrosisSerum Amyloid P-ComponentBleomycinSerum Amyloid P-Component

Identifiers

PMID24695531
PMCPMC3973556
OpenAlexW2086230499

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.