Evidence map›Paper›PMID 22058156›Full record

ReviewAmerican journal of physiology. Heart and circulatory physiology2012

Current perspectives on cardiac amyloidosis.

Jian Guan, Shikha Mishra, Rodney H Falk, Ronglih Liao

Abstract readReview
In one paragraph

Review in American journal of physiology. Heart and circulatory physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

36 citing papers in PubMed, 79 citations in OpenAlex.

  1. Trial
  2. Monoclonal gammopathy of undetermined significance in systemic transthyretin amyloidosis (ATTR).Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis · 2018
    Trial
  3. Trial
  4. Article
  5. Article
  6. Article
  7. Review
  8. Cardiac transthyretin amyloidosisEuropean journal of nuclear medicine and molecular imaging · 2021
    Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Histopathology in HCM.Global cardiology science & practice · 2018
    Review
  18. Impact of flow, gradient, and left ventricular function on outcomes after transcatheter aortic valve replacement.Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions · 2018
    Observational
  19. Article
  20. 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 2 institutions in 1 country.

Jian GuanCardiac Muscle Research Lab., 77 Ave. Louis Pasteur, NRB 431, Boston, MA 02115, USA.
Shikha Mishra
Rodney H Falk
Ronglih Liao
Brigham and Women's Hospital · USHarvard University · US

Funding

Harnessing Adult Stem Cells for Cardiac RegenerationR01HL086967 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LIAO, RONGLIH · 2007 to 2011
$2.1M
Role of Abcg2/Bcrp1 in Cardiac Side Population CellsR01HL093148 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LIAO, RONGLIH · 2008 to 2012
$2.1M
NHLBI NIH HHS HL-086967NHLBI NIH HHS HL-093148NHLBI NIH HHS HL-099173
6 · The paper itself

Abstract

Amyloidosis represents a group of diseases in which proteins undergo misfolding to form insoluble fibrils with subsequent tissue deposition. While almost all deposited amyloid fibers share a common nonbranched morphology, the affected end organs, clinical presentation, treatment strategies, and prognosis vary greatly among this group of diseases and are largely dependent on the specific amyloid precursor protein. To date, at least 27 precursor proteins have been identified to result in either local tissue or systemic amyloidosis, with nine of them manifesting in cardiac deposition and resulting in a syndrome termed "cardiac amyloidosis" or "amyloid cardiomyopathy." Although cardiac amyloidosis has been traditionally considered to be a rare disorder, as clinical appreciation and understanding continues to grow, so too has the prevalence, suggesting that this disease may be greatly underdiagnosed. The most common form of cardiac amyloidosis is associated with circulating amyloidogenic monoclonal immunoglobulin light chain proteins. Other major cardiac amyloidoses result from a misfolding of products of mutated or wild-type transthyretin protein. While the various cardiac amyloidoses share a common functional consequence, namely, an infiltrative cardiomyopathy with restrictive pathophysiology leading to progressive heart failure, the underlying pathophysiology and clinical syndrome varies with each precursor protein. Herein, we aim to provide an up-to-date overview of cardiac amyloidosis from nomenclature to molecular mechanisms and treatment options, with a particular focus on amyloidogenic immunoglobulin light chain protein cardiac amyloidosis.

Indexed as

AmyloidosisHeart DiseasesHumansMyocardiumMyocytes, Cardiac

Identifiers

PMID22058156
PMCPMC3353775
OpenAlexW2122784961

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.