What cell programs mark ischemic cardiomyopathy?
snRNA-seq of ~100k cardiac nuclei showed fewer cardiomyocytes and more specialized endothelial states in ICM, overlapping other end-stage cardiomyopathy programs.
Source
Single-nucleus RNA sequencing in ischemic cardiomyopathy reveals common transcriptional profile underlying end-stage heart failure
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
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What cell programs mark ischemic cardiomyopathy?
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>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
What they did
Profiled non-infarct LV nuclei from ICM transplant recipients and non-failing controls with snRNA-seq.
What they found
99,684 QC nuclei in 16 clusters. ICM had fewer cardiomyocytes and more lymphatic/angiogenic/arterial endothelial cells; transcriptional changes resembled HCM/DCM datasets.
The limits
What it doesn't show
End-stage transplant tissue may not represent early ICM; composition shifts are associative.
Key terms
- snRNA-seq
- Single-nucleus RNA sequencing.
- Ischemic cardiomyopathy
- Heart failure after ischemic injury/remodeling.
- Non-failing control
- Comparison hearts without end-stage failure.
- Endothelial subtypes
- Lymphatic, angiogenic, arterial EC states.
- LAMININ signaling
- ECM pathway highlighted from endothelium.
- Druggable genes
- Shared cardiomyopathy targets suggested by dataset mining.
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QC nuclei ~
Common questions
Nuclei after QC?
99,684.
Donors?
7 ICM + 8 NF.
Composition shift?
Fewer cardiomyocytes; more specialized ECs.
Cross-disease?
Similar to HCM/DCM programs.
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