Smad1 Signaling Stimulates a Regulatory Infarct Myofibroblast Subpopulation and Protects the Heart from Adverse Remodeling
Smad1 signaling stimulates a regulatory infarct myofibroblast subpopulation that protects the heart from adverse remodeling.
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Our approach grew from an award-winning discovery: spatially distinct fibroblast subpopulations that separate protective repair from harmful invasion.
Selected publications & scientific contributions
Original research and reviews
Circulation
Research
Research
Fibroblast Smad7 Induction Protects the Remodeling Pressure-Overloaded Heart
Fibroblast Smad7 restrained fibrotic remodeling in pressure-overloaded mouse hearts through regulation of fibroblast activation and matrix remodeling.
Smad7 effects on TGF-β and ErbB2 restrain myofibroblast activation and protect from postinfarction heart failure
Myofibroblast-specific Smad7 loss worsened post-infarction fibrosis and cardiac dysfunction in mice, identifying an endogenous brake on TGF-β and ErbB2 signaling.
Collagen denaturation in the infarcted myocardium involves temporally distinct effects of MT1-MMP-dependent proteolysis and mechanical tension
Mouse infarction studies and collagen-lattice experiments identified distinct contributions of proteolysis and mechanical tension to collagen denaturation during infarct healing.
Validation of diagnostic criteria and histopathological characterization of cardiac rupture in the mouse model of nonreperfused myocardial infarction
Systematic histopathology linked rupture in infarcted mouse hearts to increased macrophage influx and reduced reparative myofibroblast infiltration while defining the limits of autopsy-based diagnosis.
Macrophages in the infarcted heart acquire a fibrogenic phenotype, expressing matricellular proteins, but do not undergo fibroblast conversion
Infarct macrophages adopt a fibrogenic, matricellular-expressing phenotype without converting into fibroblasts — refining the cellular map of scar formation.
The broader scientific context
Reviews & perspectives
Decoding cardiac homeostasis and injury: the evolving landscape of spatial transcriptomics
This review maps how spatial transcriptomics resolves the cellular neighborhoods and signaling interactions that shape cardiac homeostasis, injury, and repair.
Properties and Functions of Fibroblasts and Myofibroblasts in Myocardial Infarction
This review synthesizes the changing roles and heterogeneous phenotypes of fibroblasts in inflammation, scar formation, and adverse remodeling after myocardial infarction.
The role of Smad signaling cascades in cardiac fibrosis
This review maps how Smad signaling cascades drive fibroblast activation and matrix remodeling in the injured heart — and identifies Smad-dependent responses as therapeutic targets.
These publications provide scientific context and do not establish clinical efficacy of the CorPhylaxis platform.
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