| Affiliations: |
DeBakey Executive Research Leadership Program, College of Medicine Rutkowski Lab
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| Project Leader: | Gaurav Baranwal gauravbaranwal@tamu.edu Medical Physiology |
| Faculty Mentor: | Dr. Joseph Rutkowski, Ph.D. |
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Meeting Times:
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Friday 3:30 PM-5:00 PM |
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Team Size:
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4 (Team Full) |
| Open Spots: | 0 |
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Special Opportunities:
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A great opportunity to work with three collaborative labs with different expertise: Hypertension, Microbiology and Immunology, and Lymphatic biology on a clinically-relevant question. Participants may have the potential for undergraduate research presentations and authorship recognition of their work with significant, dedicated contribution to the project.
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Team Needs:
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Those who have particular interest in physiology and in gaining experience in biology wet lab techniques. Almost 8-10 h per week commitment is preferred which includes the meeting time.
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Description:
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Hypertension (HTN) is endemic in the United States with almost 1 in 2 adults exhibiting elevated blood pressure according to recent American Heart Association guidelines. . Patients with HTN are at a 3-fold higher risk for developing cardiovascular- renal disease such as coronary artery disease, stroke, or chronic kidney disease. Current anti-hypertensive medications have numerous serious side effects, therefore there is a critical need for targeted therapies that can reduce the detrimental cardiovascular-renal effects of HTN. Previous reports have identified detrimental a role of pro-inflammatory T-cells in HTN progression. The microbiota plays a key role in a number of complex diseases, including cardiovascular disease (CVD) and HTN, largely mediated by the production of beneficial and detrimental metabolites. Work at Texas A&M has identified a class of microbial metabolites that impact T-cell inflammation. The connection between specific gut microbiota metabolites, immune cells, and HTN has not been examined extensively. In the current interdisciplinary project we are trying to understand the role of metabolites from microbiota in modulation of pro-inflammatory T-cells in HTN animal models.
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