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- W4311376459 endingPage "15814" @default.
- W4311376459 startingPage "15814" @default.
- W4311376459 abstract "Myocardial infarction (MI), a major contributor to worldwide morbidity and mortality, is caused by a lack of blood flow to the heart. Affected heart tissue becomes ischemic due to deficiency of blood perfusion and oxygen delivery. In case sufficient blood flow cannot be timely restored, cardiac injury with necrosis occurs. The ischemic/necrotic area induces a systemic inflammatory response and hundreds of thousands of leukocytes are recruited from the blood to the injured heart. The blood pool of leukocytes is rapidly depleted and urgent re-supply of these cells is needed. Myeloid cells are generated in the bone marrow (BM) and spleen, released into the blood, travel to sites of need, extravasate and accumulate inside tissues to accomplish various functions. In this review we focus on the leukocyte supply chain and will separately evaluate different myeloid cell compartments (BM, spleen, blood, heart) in steady state and after MI. Moreover, we highlight the local and systemic kinetics of extracellular factors, chemokines and danger signals involved in the regulation of production/generation, release, transportation, uptake, and activation of myeloid cells during the inflammatory phase of MI." @default.
- W4311376459 created "2022-12-25" @default.
- W4311376459 creator A5006952690 @default.
- W4311376459 creator A5007330285 @default.
- W4311376459 creator A5012230783 @default.
- W4311376459 creator A5082895910 @default.
- W4311376459 date "2022-12-13" @default.
- W4311376459 modified "2023-09-26" @default.
- W4311376459 title "Quo Vadis? Immunodynamics of Myeloid Cells after Myocardial Infarction" @default.
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