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. Author manuscript; available in PMC: 2014 Jun 10.
Published in final edited form as: J Thromb Thrombolysis. 2014 Jan;37(1):24–31. doi: 10.1007/s11239-013-1032-7

Figure 1. Sequence of events in BMSPC mobilization from the BM towards ischemic myocardium during MI.

Figure 1

Acute myocardial infarction initiates an inflammatory response resulting in the activation of the complement cascade that in turn releases proteases (by granulocytes and osteoclasts) in the BM, which proteolytically inactivate the SDF-1-CXCR4 interaction between BM osteoclasts and BMSPCS. The now mobilized BMSPCs follow an increasing SDF-1 and bioactive lipid (S1P and C1P) gradient to exit the BM niches into the PB. Acute inflammation also promotes release of cathelicidins (LL-37), which facilitate clustering of CXCR4 into lipid rafts thereby increasing their sensitivity towards lower levels of local SDF-1 in the injured myocardium. Together, the increased sensitivity towards SDF-1 and bioactive lipid gradients facilitate BMSPC homing towards ischemic myocardium.