Evidence map›Paper›PMID 21998211›Full record

ArticleBlood2011

Doxycycline reduces fibril formation in a transgenic mouse model of AL amyloidosis.

Jennifer Ellis Ward, Ruiyi Ren, Gianluca Toraldo, Pam Soohoo, Jian Guan, Carl O'Hara, Ravi Jasuja, Vickery Trinkaus-Randall, Ronglih Liao, Lawreen H Connors and 1 more

2 registry-linked trialsOpen access · bronzeAbstract read
In one paragraph

Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
3.2field-weighted citation impact, top 8% 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.

NCT01677286 phase2completednot on this mapstarted 2012, after this paper: background citation

A Phase II Study of Doxycycline in Patients With Amyloidosis

TypeinterventionalSponsorBoston UniversityRan2012 to 2015Enrolled25ConditionsAmyloidosisArmsDoxycycline 100 mg po bid x 12 months
NCT03401372 nacompletednot on this mapstarted 2018, after this paper: background citation

Comparison of Bortezomib-Cyclophosphamide-Dexamethasone Chemotherapy With or Without Doxycycline in Newly Diagnosed Mayo Stage II-III Light Chain Amyloidosis Patients: A Multi-center Randomized Controlled Trial

TypeinterventionalSponsorJian LiRan2018 to 2020Enrolled140ConditionsAmyloidosis, SystemicArmsDoxycycline, Bortezomib, Cyclophosphamide, Dexamethasone
3 · Its place in the literature

Who cites it

70 citing papers in PubMed, 150 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
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  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
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  11. Review
  12. Review
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  14. Article
  15. Review
  16. Amyloidosis of the Heart and Kidney.Methodist DeBakey cardiovascular journal · 2022
    Review
  17. Cardiac Amyloidosis Treatment.Methodist DeBakey cardiovascular journal · 2022
    Review
  18. Review
  19. Article
  20. Molecular Mechanisms of Cardiac Amyloidosis.International journal of molecular sciences · 2021
    Review

10 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

Jennifer Ellis WardAmyloid Treatment and Research Program, and Department of Medicine, Medicine, Boston University School of Medicine and Boston Medical Center, Boston, MA 02118, USA.
Ruiyi Ren
Gianluca Toraldo
Pam Soohoo
Jian Guan
Carl O'Hara
Ravi Jasuja
Vickery Trinkaus-Randall
Ronglih Liao
Lawreen H Connors
David C Seldin
Amyloidosis Foundation · USBoston University · USBrigham and Women's Hospital · US

Funding

Tissue response to amyloidogenic light chainsP01HL068705 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SELDIN, DAVID C · 2002 to 2006
$7.8M
NHLBI NIH HHS HL68705-04NHLBI NIH HHS P01 HL068705
6 · The paper itself

Abstract

Systemic AL amyloidosis results from the aggregation of an amyloidogenic immunoglobulin (Ig) light chain (LC) usually produced by a plasma cell clone in the bone marrow. AL is the most rapidly fatal of the systemic amyloidoses, as amyloid fibrils can rapidly accumulate in tissues including the heart, kidneys, autonomic or peripheral nervous systems, gastrointestinal tract, and liver. Chemotherapy is used to eradicate the cellular source of the amyloidogenic precursor. Currently, there are no therapies that target the process of LC aggregation, fibril formation, or organ damage. We developed transgenic mice expressing an amyloidogenic λ6 LC using the cytomegalovirus (CMV) promoter to circumvent the disruption of B cell development by premature expression of recombined LC. The CMV-λ6 transgenic mice develop neurologic dysfunction and Congophilic amyloid deposits in the stomach. Amyloid deposition was inhibited in vivo by the antibiotic doxycycline. In vitro studies demonstrated that doxycycline directly disrupted the formation of recombinant LC fibrils. Furthermore, treatment of ex vivo LC amyloid fibrils with doxycycline reduced the number of intact fibrils and led to the formation of large disordered aggregates. The CMV-λ6 transgenic model replicates the process of AL amyloidosis and is useful for testing the antifibril potential of orally available agents.

Indexed as

Disease Models, AnimalAdministration, OralAge FactorsAmyloidAmyloidosisAnimalsAnti-Bacterial AgentsCytomegalovirusDoxycyclineFemaleGastric MucosaHumansImmunoblottingImmunoglobulin Light-chain AmyloidosisImmunoglobulin Light ChainsImmunohistochemistryAmyloidAnti-Bacterial AgentsDoxycyclineImmunoglobulin Light Chains

Identifiers

PMID21998211
PMCPMC3242721
OpenAlexW2069180940

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.