Summary of project PR002468
This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR002468. The data can be accessed directly via it's Project DOI: 10.21228/M8MR7Q This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
| Project ID: | PR002468 |
| Project DOI: | doi: 10.21228/M8MR7Q |
| Project Title: | Host sensing of microbially produced imidazole propionate is a driver and therapeutic target in atherosclerosis |
| Project Summary: | Atherosclerosis is the main underlying cause of cardiovascular diseases (CVDs). Its prevention is based on the detection and treatment of traditional cardiovascular risk factors but often fails to identify individuals at risk for early vascular disease. Recent research has suggested new players in the pathophysiology of atherosclerosis, highlighting the need for alternative disease biomarkers and therapeutic targets to improve early diagnosis and therapy efficacy. Here, we identified that microbially produced imidazole propionate (ImP) is associated with the extent of atherosclerosis in mice and in two independent human cohorts. Furthermore, ImP administration to atherosclerosis-prone mice fed chow diet was sufficient to induce atherosclerosis without altering the lipid profile, and it was linked to activation of both systemic and local innate and adaptive immunity and inflammation. Specifically, we found that ImP caused atherosclerosis through Imidazoline-1 receptor (I1R) expressed in myeloid cells. Blocking this ImP/I1R axis inhibited the development of atherosclerosis induced by ImP as well as by high cholesterol diet in mice. Identification of the strong association of ImP with active atherosclerosis, along with the discovery of the contribution of the ImP/I1R axis to disease progression opens new avenues for improving the early diagnosis and personalized therapy of atherosclerosis. |
| Institute: | University of Gothenburg |
| Last Name: | Beck |
| First Name: | Katharina |
| Address: | Bruna Straket 16, Gothenburg, Sweden, 41345, Sweden |
| Email: | katharina.beck@wlab.gu.se |
| Phone: | 7803084 |
Summary of all studies in project PR002468
| Study ID | Study Title | Species | Institute | Analysis(* : Contains Untargted data) | Release Date | Version | Samples | Download(* : Contains raw data) |
|---|---|---|---|---|---|---|---|---|
| ST003938 | Host sensing of microbially produced imidazole propionate is a driver and therapeutic target in atherosclerosis | Homo sapiens | University of Gothenburg | MS | 2025-06-25 | 1 | 1844 | Uploaded data (48.8M)* |
