Key result
Mfge8 deficiency accelerates atherosclerosis by impairing clearance of apoptotic debris in mice.
Why the study?
Key factors responsible for maintaining immune regulation in the proinflammatory milieu of atherosclerosis are poorly understood.
Population
Murine model of atherosclerosis with bone marrow-derived Mfge8 disruption
Comparison
Mfge8 deficiency vs normal Mfge8 expression in bone marrow-derived cells
Design
Experimental study in mice
Authors
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Hypothesis-generating for Mfge8 in human atherosclerosis; prospective studies needed before clinical consideration.
Lactadherin (Mfge8) plays a crucial role in clearing apoptotic cells and regulating the immune response to prevent accelerated atherosclerosis.
Ait‐Oufella et al. (2007) studied Atherosclerosis. Disruption of bone marrow-derived Mfge8 (lactadherin deficiency) vs. Normal Mfge8 expression was evaluated on Atherosclerosis development and apoptotic cell accumulation. Disruption of bone marrow-derived Mfge8 in a murine model led to substantial accumulation of apoptotic debris and marked acceleration of atherosclerosis.
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