Promoting Inflammation Resolution Response as a Therapeutic Strategy in Atherosclerosis

posted Jan 25, 2017, 11:11 PM by sourav ghosh
Manikandan Subramanian 
MBBS, PhD, Senior Scientist and Ramalingaswami Fellow, CSIR-Institute of Genomics & Integrative Biology, New Delhi, India

Atherosclerosis is a non-resolving chronic inflammatory disease triggered by the sub-endothelial retention of lipoproteins in large and medium-sized arteries. A small proportion of these atherosclerotic plaques display a “vulnerable phenotype” characterized by large necrotic cores and thin fibrous cap, which are harbingers of plaque rupture and acute luminal thrombosis leading to clinical conditions such myocardial infarction and stroke. Our studies have established that the dominant cellular processes that lead to vulnerable plaque development are 1) increased atherosclerotic lesional cell apoptosis, 2) defective phagocytic clearance of apoptotic cells (efferocytosis), and 3) failed inflammation resolution. Over the past few years, our research has focused on unraveling the mechanistic basis of these molecular events with a particular emphasis on the role of innate-adaptive immune cell interactions and inflammatory cytokine cross-talk in shaping these processes. Most recently, using a nanomedicine approach, we have demonstrated the possibility of enhancing efferocytosis efficiency within the atherosclerotic plaque to promote inflammation resolution and stabilization of advanced plaques.

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