Modulation of Macrophage Function through Alternative Splicing in Cardiometabolic Diseases

Project: Research project

Project Details


Systemic chronic inflammation seen in cardiometabolic diseases, which confer significant morbidity and mortality worldwide, can induce macrophages to shift toward a pro-inflammatory phenotype in disease relevant tissues, e.g., the arterial wall in atherosclerosis. The mechanistic underpinnings of how macrophages shift phenotypes, an area for possible therapeutic targeting, remain incompletely understood; and a missing link is whether alternative splicing, which generates multiple protein isoforms, also contributes to the function of key proteins directly relevant to macrophage phenotypes and disease-relevant functions. The research outlined in this proposal will shed light on the possibility that alternative splicing modulates macrophage phenotype and function, providing a translational framework for future therapeutic targeting of the cardiometabolic diseasepromoting, pro-inflammatory macrophage.
Effective start/end date8/1/187/31/21


  • National Heart, Lung, and Blood Institute (5K08HL135348-04)


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