Key result
This review highlights the mechanisms of chemokine-mediated leukocyte recruitment in atherosclerosis and the immune-inflammatory response post-myocardial infarction in experimental models.
This review highlights the mechanisms of chemokine-mediated leukocyte recruitment in atherosclerosis and post-myocardial infarction based on experimental models.
Offers no immediate clinical guidance; leaves open translation of chemokine pathways from experimental models to human atherosclerosis and post-MI care.
Chemokine-induced leukocyte migration into the vessel wall is an early pathological event in the progression of atherosclerosis, the underlying cause of myocardial infarction. The immune-inflammatory response, mediated by both the innate and adaptive immune cells, is involved in the initiation, recruitment, and resolution phases of cardiovascular disease progression. Activation of leukocytes via inflammatory mediators such as chemokines, cytokines, and adhesion molecules is instrumental in these processes. In this review, we highlight leukocyte activation with the main focus being on the mechanisms of chemokine-mediated recruitment in atherosclerosis and the response postmyocardial infarction with key examples from experimental models of cardiovascular inflammation.
No takes yet. Share an insight, caveat, or question.
Jones et al. (2017) conducted a review in Cardiovascular disease (atherosclerosis, myocardial infarction). Leukocyte trafficking and chemokine-mediated recruitment was evaluated. This review highlights the mechanisms of chemokine-mediated leukocyte recruitment in atherosclerosis and the immune-inflammatory response post-myocardial infarction in experimental models.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: