Sayed Lab · Stanford University

Engineering Human Cardiovascular Models to Understand Disease and Discover New Therapies

We integrate patient-derived biospecimens, human iPSCs, multicellular cardiovascular models, genome engineering, and single-cell and spatial multi-omics to uncover mechanisms of cardiovascular disease.

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Endothelial
Network

Cardiac
Organoid

Single-Cell
Multi-omics

Spatial
Transcriptomics

From Patients to Therapies

Patients &
Biobank

iPSCs

Cardiovascular
Cells

Organoids &
Engineered Tissues

Single-Cell & Spatial
Multi-Omics

Mechanisms

Therapeutic
Interventions

Our Research

Multicellular Approaches. Human Impact.

Cardiomyopathy and heart failure illustration

Cardiomyopathy & Heart Failure

Defining multicellular mechanisms of inherited and acquired cardiomyopathy and identifying pathways that drive myocardial dysfunction, remodeling, and heart failure.

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Vascular biology and regeneration illustration

Vascular Biology & Regeneration

Investigating endothelial function, vascular remodeling, endothelial plasticity, and regenerative mechanisms in health and disease.

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Precision Cardio-Oncology

Uncovering mechanisms of cancer therapy-associated cardiotoxicity and developing precision cardioprotective strategies using patient-specific human models.

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Functional Cardiovascular Genomics

Using genome engineering, CRISPR-based functional genomics, and multi-omics to identify causal variants and regulatory pathways that drive cardiovascular disease.

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Environmental Cardiovascular Disease

Studying how environmental exposures and gene-environment interactions influence vascular and cardiac dysfunction using human experimental models.

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Single-cell and spatial multi-omics illustration

Single-Cell & Spatial Multi-Omics

Resolving disease-associated cell states, regulatory programs, and spatially organized pathways at cellular resolution.

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Aging and cardiovascular disease illustration

Aging & Cardiovascular Disease

How biological aging reshapes vascular and cardiac health.

We investigate how aging alters inflammatory signaling, endothelial function, vascular integrity, cellular state, and cardiac performance. Our work integrates human data, computational approaches, and iPSC-based cardiovascular models to define mechanisms of cardiovascular aging.

We are particularly interested in how aging intersects with genetic susceptibility, environmental stressors, and chronic inflammation to influence cardiovascular resilience and disease progression.

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A Human-Centered Approach

From patients to mechanisms to therapies.

Our research is grounded in patient samples and clinical phenotypes, combined with advanced human models to ensure biological relevance and translational impact.

Patients &
Biospecimens

iPSCs

Multicellular
Models

Molecular
Mechanisms

Therapeutic
Discovery