Posts Tagged: macrophage ontogeny

Resident and Monocyte-Derived Macrophages in Cardiovascular Disease

Resident and Monocyte-Derived Macrophages in Cardiovascular Disease

Lisa Honold, Matthias Nahrendorf

Macrophage mediators and crosstalk after myocardial infarction. TNF-α (tumor necrosis factor α) acts on cardiomyocytes and can induce hypertrophy and cell death. TGF-β (transforming growth factor-β) induces conversion of fibroblasts to myofibroblasts that produce collagen necessary for scar formation. Proteolytic enzymes like MMPs (matrix metalloproteinases) contribute to tissue remodeling, whereas VEGF (vascular endothelial growth factor) acts on endothelial cells and stimulates angiogenesis. [Powerpoint File]

Resident and Monocyte-Derived Macrophages in Cardiovascular Disease

Resident and Monocyte-Derived Macrophages in Cardiovascular Disease

Lisa Honold, Matthias Nahrendorf

Macrophages in cardiovascular disease. During myocardial infarction (MI), atherosclerosis and stroke, monocytes are supplied by medullary and extramedullary hematopoiesis in bone marrow and spleen. Monocytes infiltrate diseased tissues, differentiate into macrophages and proliferate locally. In MI, resident cardiac macrophages are lost, whereas arterial macrophages in atherosclerosis persist. Cerebral microglia are activated after stroke and contribute to disease progression and healing. In obesity, macrophage accumulation in adipose tissue stems from local proliferation of resident and recruitment of monocyte-derived macrophages. [Powerpoint File]