Macrophage inflammation; cellular identity and healthspan during aging
Macrophages are critical mediators of inflammaging, cellular senescence and metabolic impairments, ultimately leading to a loss of cellular identity and declining healthspan during aging. Aging is also associated with altered epigenomics and chromatin accessibility. Understanding the age-specific macrophage signals that imprint cellular memory, causing loss of identity, could generate therapeutic candidates that eliminate the imprinting and permit return to homeostasis. Dr. Camell proposes to investigate the consequence of macrophage signals on histone modifications that imprint cellular memory in metabolic and lymphoid organs. Her lab will investigate the resulting inflammation, cellular senescence and fibrosis that lead to metabolic dysfunction.