Fernando Camargo
Boston Children's Hospital
Karp Building, 6th Floor, Room 06127
One Blackfan Circle
Boston, MA 02115
The Camargo Lab is focused on understanding how stem cells build, maintain, and repair tissues, and how these processes go awry in disease. We develop and apply cutting-edge technologies that allow us to study cell fate decisions in their native environment, at single-cell resolution. By integrating lineage tracing, single cell -omics, and functional biology, we are uncovering how blood and liver cells are generated, maintained, and remodeled during development, aging, and disease.
A central goal of our work is to explain why the blood and immune system decline with age, leading to reduced immune competence, impaired response to infection, and increased cancer risk. We are also studying how liver cells can be reprogrammed for regenerative purposes, with the goal of enhancing tissue repair in chronic liver disease. In both systems, we seek to translate basic insights into new therapeutic strategies, ranging from improving bone marrow transplantation to developing regenerative interventions for liver failure and fibrosis.
Potential research projects:
- Development of single-cell lineage tracing tools to follow individual stem and progenitor cells in their native tissue context
- Integration of single-cell genomics and lineage information to define molecular programs of cell fate and dysfunction
- Spatial transcriptomics approaches in development to map how cell fate and clonal dynamics are influenced by tissue architecture
- Genetic and functional screens in vivo to identify regulators of hematopoietic aging, immune decline, and malignant transformation
- Dissecting developmental origins of hematopoiesis to understand how embryonic progenitors shape lifelong blood production
- Mechanisms of hepatocyte plasticity and reprogramming, including epigenetic “brakes” on fate change that can be targeted to enhance regeneration
- Hippo/YAP signaling in liver regeneration and cancer, defining how regenerative programs can be activated without triggering tumorigenesis