Gene expression
What cell programs mark ischemic cardiomyopathy?
Open access · cc by · source: Europe PMC
snRNA-seq of ~100k cardiac nuclei showed fewer cardiomyocytes and more specialized endothelial states in ICM, overlapping other end-stage cardiomyopathy programs.
How this study connects
Role on claims
Each row is a claim on a concept or method page where this paper supports, challenges, or qualifies the statement. Roles are hand-checked — not a model guess.
snRNA-seq maps end-stage ischemic cardiomyopathy cell states.
Profiling ~100k human cardiac nuclei showed fewer cardiomyocytes and more specialized endothelial states in ICM versus non-failing controls, with programs overlapping other end-stage cardiomyopathies.
Evidence for the claim as stated.
Disease atlases depend on QC’d nuclei before cell-state claims.
ICM snRNA-seq profiles ~100k QC’d cardiac nuclei before composition claims—reminding students that atlas biology sits atop filtering decisions.
Evidence for the claim as stated.
A mito-filter methods result, a foundation-model benchmark, and a disease atlas answer different layers of the single-cell stack.
Evidence for the claim as stated.
Open questions
Tensions this paper is part of
From concept pages' “where studies disagree.” Disagreement means the same question; scope means different assays, populations, or outcomes.
A mito-filter methods result, a foundation-model benchmark, and a disease atlas answer different layers of the single-cell stack.
History
When this study was placed
Dated entries from the concept change log — when this paper was added or removed as support, challenge, or qualifier on a claim.
Placed as supporting evidence on Single-cell RNA-seq (scRNA-seq)
Profiling ~100k human cardiac nuclei showed fewer cardiomyocytes and more specialized endothelial states in ICM versus non-failing controls, with programs overlapping other end-stage cardiomyopathies.
Placed as supporting evidence on Single-cell RNA-seq (scRNA-seq)
Profiling ~100k human cardiac nuclei showed fewer cardiomyocytes and more specialized endothelial states in ICM versus non-failing controls, with programs overlapping other end-stage cardiomyopathies.
Study at a glance
- Design
- Case-control — snRNA-seq of non-infarct LV from ICM transplant recipients vs NF controls
- N
- N=15 · 7 ICM + 8 NF; 99,684 nuclei after QC
- Population
- Human LV nuclei from ICM and non-failing hearts
- Outcome
- Cell-composition and transcriptional differences in ICM vs NF
Structured fields used in claim comparison tables when every cited study has a complete layer.
Inspect source passages
What cell programs mark ischemic cardiomyopathy?
These passages occur verbatim in the stored paper text. They support the points listed below; they do not verify every statement in the explanation.
>99,000 nuclei from 7 ICM and 8 NF.
Using single-nucleus RNA sequencing (snRNA-seq) and integrated computational analyses, we profile the transcriptomes of over 99,000 human cardiac nuclei from the non-infarct region of the left ventricle of 7 ICM transplant recipients and 8 non-failing (NF) controls.
99,684 QC nuclei.
oval of low-quality nuclei, 99,684 nuclei (39,339 ICM; 60,345 NF) across 16 clusters remained ( Figures 1A
Key findings
99,684 QC nuclei in 16 clusters. ICM had fewer cardiomyocytes and more lymphatic/angiogenic/arterial endothelial cells; transcriptional changes resembled HCM/DCM datasets.
Methodology
Profiled non-infarct LV nuclei from ICM transplant recipients and non-failing controls with snRNA-seq.
Limitations
End-stage transplant tissue may not represent early ICM; composition shifts are associative.
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