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Seven Hundred Fifty Thousand Cells Redraw Heart Failure
A single-cell atlas linked noncoding risk regions to regulatory changes across the healthy and failing human heart.
Summary
A single-cell atlas linked noncoding risk regions to regulatory changes across the healthy and failing human heart.
UC San Diego-led researchers integrated gene activity, chromatin accessibility, and three-dimensional genome organization in more than 750,000 cells from 36 human hearts. They mapped 12 major cardiac cell types and found heart failure associated with more fibroblasts and immune cells, fewer cardiomyocytes, and cell-specific regulatory shifts. The atlas proposes targets and causal pathways for testing; it is a resource for discovery, not a therapy.
Why it matters
A single-cell atlas linked noncoding risk regions to regulatory changes across the healthy and failing human heart.
Limits and context
- The atlas proposes targets and causal pathways for testing; it is a resource for discovery, not a therapy.
Key claims
A single-cell atlas linked noncoding risk regions to regulatory changes across the healthy and failing human heart.
Qualification: The atlas proposes targets and causal pathways for testing; it is a resource for discovery, not a therapy.
Evidence: source-2026-07-24-007
Sources
- UC San Diego via Newswise: Heart-failure gene regulation mapUC San Diego via Newswise · secondary reporting
Corrections
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