Evidence map›Paper›PMID 42804833›Full record

ArticleJACC. Basic to translational science2026

The Role of Cardiac Fibrosis and Fibroblast Activation in Amyloid Light Chain (AL) Amyloidosis.

Shingo Narita, John Isaiah Jimenez, Nixuan Cai, Hiroki Kitakata, Sharmila Dorbala, Y Joseph Woo, Kevin M Alexander, Ronglih Liao

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in JACC. Basic to translational science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Shingo NaritaStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, California, USA; Department of Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California, USA. Electronic address: naritas@stanford.edu.
John Isaiah JimenezStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, California, USA; Department of Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California, USA.
Nixuan CaiStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, California, USA; Department of Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California, USA.
Hiroki KitakataStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, California, USA; Department of Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California, USA.
Sharmila DorbalaCardiac Amyloidosis Program, Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA; Division of Nuclear Medicine and Molecular Imaging, Department of Radiology, Brigham and Women's Hospital, Boston, Massachusetts, USA; CV Imaging Program, Cardiovascular Division and Department of Radiology, Brigham and Women's Hospital, Boston, Massachusetts, USA.
Y Joseph WooStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, California, USA; Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, California, USA.
Kevin M AlexanderStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, California, USA; Department of Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California, USA; Stanford Amyloid Center, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California, USA.
Ronglih LiaoStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, California, USA; Department of Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California, USA; Stanford Amyloid Center, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California, USA. Electronic address: rliao7@stanford.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies suggest that interactions between collagen and amyloid fibril may influence amyloid formation, matrix remodeling, and disease progression in cardiac amyloid light chain (AL) amyloidosis. However, the precise pathophysiological mechanisms underlying fibrosis remain largely unexplored. Here, we performed transcriptome analysis of myocardial samples from patients with AL amyloidosis and identified upregulation of fibroblast activation genes, such as collagen type I/III and periostin. Histology showed predominantly type III collagen fibrosis, accompanied by cardiac fibroblasts present within the interstitial myocardium, including areas with amyloidogenic light chain (AL-LC). We further demonstrated a partial fibroblast-to-myofibroblast transition (FMT) in vitro by stimulating cardiac fibroblasts with AL-LC. This indicates that pathogenic AL-LC directly induces fibroblast activation and that matrix remodeling accelerates during amyloid fibril deposition. This extensive cellular and molecular characterization provides novel insights into the essential role of fibrotic pathology in AL cardiomyopathy and may enable the discovery of biomarkers and therapeutic targets.

Indexed as

AL cardiomyopathycardiac AL amyloidosiscardiac fibrosisfibroblast activationheart failure

Identifiers

PMID42804833
PMCPMC13546838

What OpenQuestion holds

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Registered trials

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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.