The abstract is read at the publisher; the summary is JClub's.
Lymphatic endothelial cells instruct reverse cardiac remodeling in a reversible murine pressure-overload model, and lymphatic-derived Reelin (RELN) suppresses pathological fetal gene activation in cardiomyocytes.
- Why it matters: Mechanical unloading can improve heart failure, but recovery is often incomplete and the multicellular mechanisms that constrain it are unclear.
- What they did: The study used a reversible murine pressure-overload model with bulk and single-nucleus transcriptomics, plus multicellular factor and cell-cell communication analyses, to link recovery programs to specific cell types and factors.
- The result: Unloading improved cardiac function and partially restored extracellular matrix and metabolic programs, yet inflammatory and mitochondrial dysfunction signatures persisted; RELN directly suppressed fetal gene activation in murine and human cardiomyocytes.
The findingWhy it mattersWhat they didThe result
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