Evidence map›Paper›PMID 21224044›Full record

ArticleThe American journal of pathology2011

Evidence for a functional role of the molecular chaperone clusterin in amyloidotic cardiomyopathy.

Michael J Greene, Flora Sam, Pamela T Soo Hoo, Rupesh S Patel, David C Seldin, Lawreen H Connors

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Current and Emerging Therapies for Hereditary Transthyretin Amyloidosis: Strides Towards a Brighter Future.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
    Review
  10. Article
  11. Article
  12. Modulation of the Mechanisms Driving Transthyretin Amyloidosis.Frontiers in molecular neuroscience · 2020
    Review
  13. Article
  14. Clusterin protects neurons against intracellular proteotoxicity.Acta neuropathologica communications · 2017
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

Michael J GreeneDepartment of Pathology, Boston University School of Medicine, Boston, Massachusetts, USA.
Flora Sam
Pamela T Soo Hoo
Rupesh S Patel
David C Seldin
Lawreen H Connors
Boston University · US

Funding

Role of Aldosterone in Cardiac RemodelingR01HL079099 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SAM, FLORA · 2005 to 2009
$1.8M
Molecular mechanism of senile cardiac amyloidosisR01AG031804 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI CONNORS, LAWREEN H. · 2009 to 2013
$1.6M
Follistatin-like 1 and the cardiac secretome in human heart failureR21HL102631 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SAM, FLORA · 2010 to 2011
$448k
Novel Insights into the Pathogenesis of Light Chain Cardiac AmyloidosisR21HL095891 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SAM, FLORA · 2010 to 2011
$447k
NHLBI NIH HHS HL079099NHLBI NIH HHS HL095891NHLBI NIH HHS HL102631NHLBI NIH HHS R01 HL079099NHLBI NIH HHS R21 HL095891NHLBI NIH HHS R21 HL102631NIA NIH HHS R01 AG031804NIA NIH HHS R01AG031804
6 · The paper itself

Abstract

Molecular chaperones, including the extracellular protein clusterin (CLU), play a significant role in maintaining proteostasis; they have a unique capacity to bind and stabilize non-native protein conformations, prevent aggregation, and keep proteins in a soluble folding-competent state. In this study, we investigated amyloid-infiltrated cardiac tissue for the presence of CLU and measured serum levels of CLU in patients with and without amyloidotic cardiomyopathy (CMP). Cardiac tissues containing amyloid deposits composed of either transthyretin (TTR) or Ig light chain from nine patients with amyloidotic CMP were examined for the presence of CLU using immunohistochemical techniques. CLU staining coincided with the extracellular myocardial amyloid deposits in tissues from patients with familial TTR, senile systemic, and Ig light chain amyloidosis. The association of CLU with cardiac amyloid deposits was confirmed by immunogold electron microscopy. Serum concentrations of CLU were measured in familial TTR, senile systemic, and Ig light chain amyloidosis patient groups and compared with both age-matched healthy controls and with patients with CMP unrelated to amyloid disease. Subset analysis of disease cohorts, based on cardiac involvement, indicated that decreased serum CLU concentrations were associated with amyloidotic CMP. Taken together, these results suggest that CLU may play a pathogenetic role in TTR and Ig light chain amyloidoses and amyloidotic CMP.

Indexed as

AgedAged, 80 and overAmyloidosis, FamilialCardiomyopathiesClusterinHumansImmunoglobulin Light ChainsImmunohistochemistryMiddle AgedMolecular ChaperonesPrealbuminCLU protein, humanClusterinImmunoglobulin Light ChainsMolecular ChaperonesPrealbumin

Identifiers

PMID21224044
PMCPMC3070592
OpenAlexW2128021263

What OpenQuestion holds

Textmetadata
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.