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Type 2 diabetes impact on dysregulated immune cell function in cardiovascular diseases
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26-130-2
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Type 2 diabetes impact on dysregulated immune cell function in cardiovascular diseases
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Dr. Beiyan Zhou
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Type 2 diabetes (T2DM) is the leading cause of many serious health complications, including cardiovascular diseases, chronic kidney diseases, blindness, and several types of cancers. One of the primary disease-causing factors is malfunction of the immune system, which can lead to weakened immune cell function in fighting infections and sustained low-grade systemic chronic inflammation. Through direct and indirect effects, T2DM dysregulated immune cells are pathogenic factors in various disease conditions, including atherosclerosis, infection, autoimmune diseases, and cancerous transformation. T2DM is a primary cause for the marked increase of atherosclerotic cardiovascular disease (ASCVD), accounting for 30% of symptomatic cases. Accordingly, the ASCVD risk in T2DM patients is 2-4 fold more than that in the non-T2DM population. The concomitant increase of T2DM and ASCVD in the US has prompted the urgency for more accurate ASCVD risk assessment and an effective mitigation strategy direction. Current standard-of-care therapies, addressing factors such as lipid/hypertension/glycemic control, have underachieved as indicated by recent clinical trials and extensive cohort studies. Even novel drug classes approved for ASCVD prevention in T2DM, such as SGLT2 inhibitors or GLP-1 receptor agonists, reduce disease risk by only 2%. These results warrant a new direction in the mitigation strategy, which relies on advancing our understanding of immune cell function in T2DM and T2DM-associated ASCVD. Given the volatile and central roles of monocytes in ASCVD development and progression, we recently developed a set of new algorithms to annotate their function under complex conditions with high resolution. Importantly, powered by these tools, two distinct macrophage-derived foam cell development programs were revealed (homeostatic vs. pathogenic foaming). However, mechanisms underlying T2DM-altered monocyte-derived macrophage function in ASCVD pathogenesis remain elusive. This project aims to investigate cellular and molecular mechanisms derailed by T2DM in circulating immune cells; thus, samples from healthy or T2DM patients with or without cardiovascular diseases will be needed for this study. After completing this study, we may identify new molecular targets or develop comprehensive treatments for T2DM patients to reduce their risk of comorbidities, including ASCVD.
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Cardiovascular (Heart, High Blood Pressure, Etc.)
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Diabetes
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Healthy Volunteer
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Check with study contact
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Heather Vargas. Tel.: 860-679-1658. Email: hvargas@uchc.edu
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Enrolling/recruiting. For current recruitment status, please check with study contact.
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